Andras Perl, MD, PhD

A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Phase 3 Study to Evaluate the Efficacy and Safety of BIIB059 in Adult Participants with Active Systemic Lupus Erythematosus Receiving Background Nonbiologic Lupus Standard of Care. 230LE303
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A Phase 1B, Multicenter, Open-Label, Dose-Escalation Study to Evaluate the Safety Tolerability, Pharmacokinetics, and Pharmacodynamics of Subcutaneously Administered Mosentuzumab to Participants with Systemic Lupus Erythematosus. GA43191
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Systemic Lupus Erythematosus (SLE) Treatment with N-acetylcysteine (NAC) (SNAC)
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Molecular Biology and Pathology of Transaldolase
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ROLE of HTLVS and related endogenous sequences in autoimmune diseases and human cancers
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Medicine

Rheumatology

Genes and Viruses Predisposing to Autoimmunity, Genetics, Apoptosis, Endogenous Retroviruses, and Transaldolase

• Biochemistry and Molecular Biology
• Biomedical Sciences Program
• Medicine
• Microbiology and Immunology

Overview of Contribution to Science. My research has been focused on the contribution of genetic and environmental factors in shaping immune response with a focus on autoimmunity. In search of potential genetic interactions between the host and the environment, we identified HRES-1, a human T-cell leukemia virus-related endogenous retrovirus (1), mapped it to chromosome 1q42 (2) and identified Rab4a as its gene product that confers modulates susceptibility HIV infection via increased recycling of surface receptors, such as CD4 and transferrin receptor (CD71) (3). Polymorphic haplotypes of the HRES-1 endogenous retrovirus are associated with development and disease manifestations of in patients with SLE (4). The overexpression of Rab4A gene product of HRES-1, which is detectable in T cells of SLE patients and in all lupus-prone strains prior to disease onset, also contributes to oxidative stress and mTOR activation by inhibiting mitochondrial turnover via autophagy, also called mitophagy (5). This newly uncovered pathway to lupus pathogenesis can also be exploited for therapeutic intervention through blocking the enzymatic activity of the Rab GTPases, such as Rab4A using 3-PEHPC (5). The above discoveries have been published in 170 original peer-reviewed papers, authored chapters in rheumatology and immunology textbooks. Our work has been widely cited andcredited, and inspired a recent explosion of research on the role of metabolic pathways in the pathogenesis of lupus (6-9) and other rheumatic diseases (10,11).

My laboratory has opened up the field of metabolic control of T-cell activation and lineage specification which underlie disease development both in murine models and patients with SLE (12,13). We have originally identified and cloned transaldolase, an enzyme of the pentose phosphate pathway (14), as a regulator of glutathione (GSH) metabolism (15,16) and a newly described metabolic checkpoint of T-cell activation and death signal processing: elevation of the mitochondrial transmembrane potential or, as newly termed, mitochondrial hyperpolarization (MHP) (17). As we also uncovered, persistent MHP is a critical metabolic defect in lupus T cells, which characterizes mitochondrial dysfunction and ATP depletion and predisposes to cell death by necrosis (18). The increased production of necrotic materials from T cells is an important activator of B cells and dendritic cells and leads to inflammation in SLE (19). As we have also unveiled, the depletion of intracellular glutathione (GSH) underlies mitochondrial dysfunction and MHP in lupus T cells (18). To translate these new laboratory findings into clinical practice, we directly targeted the metabolic checkpoint of GSH depletion with N-acetylcysteine (NAC), an amino acid precursor of GSH, within the context of an FDA-approved double-blind placebo-controlled interventional trial (20). Relative to placebo, orally administered NAC reversed GSH depletion and showed remarkable safety, and it reduced disease activity in SLE patients (20,21). The clinical efficacy of NAC was mediated via blockade of complex 1 of the mechanistic target of rapamycin (mTOR), which serves as a sensor of MHP and effector of pro-inflammatory T cell lineage specification in SLE. As recently reviewed (13,22), the significance of mTOR activation is relevant for autoimmune diseases beyond SLE, it effects inflammation and overall lifespan. Based on our discovery of mTOR activation in SLE (23), we have also evaluated the clinical efficacy of rapamycin and found it to be a remarkably effective therapeutic intervention in SLE patients with resistance or intolerance to immunosuppressive medications, which has been repeatedly documented (22,24). Our findings on clinical efficacy of rapamycin have been corroborated by several recent publications, as recently reviewed (25).

Our parallel studies in mouse models led to the discovery of transaldolase (TAL) deficiency as cause of inflammatory liver disease, which begins with steatohepatitis and progresses to hepatocellular carcinoma (HCC) (26). TAL deficiency has been documented as a cause of liver cirrhosis and cancer in patients as well, as recently reviewed (27). Interestingly, TAL is overexpressed in T cells of SLE patients, which may be related to protection against oxidative stress (23). The involvement of TAL in lupus pathogenesis is further supported by its increased expression in livers and spleen of MRL/lpr mice (28). Therefore, we examined whether oxidative stress, which emanates from the liver, can activate mTORC1 and thus predispose to aPL. Mitochondria from liver of mice lacking TAL (TAL-/-) exhibited increased electron transport chain (ETC) activity and activation of mTORC1. In accordance with an underlying role for oxidative stress and mTORC1 activation in the liver, the production of antiphospholipid antibodies (aPL) is increased in TAL-/- mice relative to TAL+/+ controls matched for age and gender. Importantly, rapamycin treatment abrogated the production of both anti-cardiolipin antibodies (ACLA) and anti-β2 glycoprotein I autoantibodies (anti-β2GPI) in TAL-/- mice. Likewise, aPL production was also blocked by rapamycin in lupus-prone mice (28). The remarkable efficacy of rapamycin in abrogating aPL production has immense relevance for treatment of patients with APS who currently require life-long anticoagulation (29).

Importantly, mild liver disease, defined as ≥2-fold elevation of aspartate aminotransferase or alanine aminotransferase, is associated with the production of aPL in our SLE cohort (30) as well as in previous meta-analyses (31,32). Along these lines, HCC develops in the liver following chronic inflammation, which is driven by mitochondrial oxidative stress (26,27) and responds to treatment with rapamycin (33). The growing evidence that mTORC1 blockade by rapamycin extends life expectancy (34) argues for the overall safety and benefit of this intervention. Given that aPL may precede clinical disease in patients with SLE (35,36), the underlying role of liver disease and preventative treatment via blockade of mTORC1 clearly open additional new avenues of research and patient care.

Of note, TAL is a rate-limiting enzyme of the pentose phosphate pathway (27). Deficiency of another PPP enzyme, glucose 6-phosphate dehydrogenase (G6PD), represents the most common genetic defect in humans, which affects 400 million people globally (37). Deficiency of G6PD elicits the depletion of NADPH in red cells and predisposes to oxidative stress-induced hemolytic anemia (37). The high prevalence of G6PD deficiency is attributed to its protective effects against malaria (38). In contrast to G6PD, TAL is not expressed in red cells, which lack mitochondria (39), and TAL deficiency does not cause hemolytic anemia in men or mice. However, the protozoan replicates in the liver, causes hepatitis (40,41), and induces aPL production (42). Therefore, the potential roles of TAL and the PPP as protectors from malaria would be important to determine.

As described in the above overview, my research has been dedicated to 1) uncovering the molecular basis of immune health, autoimmunity, and lupus pathogenesis, and 2) identifying metabolic checkpoints of regulatory impact which can be validated in mechanistic clinical trials. To present specific discoveries and ongoing efforts, I have grouped them into four focused categories:

1. Discovery of the HRES-1 human endogenous retrovirus and the impact of its HRES-1/Rab4 gene product on T-cell activation and lupus pathogenesis

We have identified the HRES-1, the first human endogenous retrovirus (1) which is expressed on the RNA (1) and protein levels (43), exhibits polymorphic alleles conferring susceptibility to human lupus (44). HRES-1 is centrally located within the 1q42 locus associated with lupus susceptibility in 4 independent genome-wide screens of lupus families. Polymorphic haplotypes of HRES-1 are associated with the development of glomerulonephritis in SLE (4). The impact of HRES-1 on altered T cell signaling in SLE is mediated through the HRES-1/Rab4 protein that regulates surface expression of CD4 via endocytic recycling (3). HRES-1/Rab4 regulates assembly and recycling of key components of the T-cell synapse, including T-cell receptor/CD3ζ, and corresponds to the lupus susceptibility gene at 1q42 (23). HRES-1/Rab4A (recently designated by NCBI as Rab4A: http://www.ncbi.nlm.nih.gov/gene/5867) is markedly overexpressed in lupus T cells: 3.7-fold in CD4 T cells of SLE patients (23) as well as 3.6-fold in NZB/WF1 mice and 4.7-fold in MRL/lpr mice at 4 weeks of age, before the appearance of ANA or any sign of disease (5). As a member of the Ras-like Rab small GTPase family, HRES-1/Rab4regulates endosome recycling. In particular it targets the surface proteins CD4 (3), CD71 (transferrin receptor) (3), CD2AP, and CD3ζ (23) and the intracellular protein dynamin-related protein 1 (Drp1) for lysosomal degradation (5). Drp1 plays an essential role in triggering mitochondrial fission and mitochondrial autophagy (mitophagy) (45). Therefore, the HRES-1/Rab4-mediated depletion of Drp1 causes the accumulation of mitochondria, which generate oxidative stress, both in patients and mice with SLE (5). Of note, treatment with Rab GTPase inhibitor 3-PEHPC, which inactivates Rab4A in vitro, reverses the accumulation of mitochondria, blocks ANA production and nephritis in MRL/lpr mice in vivo (5). HRES-1/Rab4 increases the very formation of autophagosomes (46). It is proposed that HRES-1/Rab4-mediated blockade of autophagy prevents the restoration of T-cell activation-induced metabolic changes in lupus T cells (47). Activation of endogenous retroviral elements, such as HRES-1 and LINE elements, contribute to the pathogenic interferon response in SLE (48). Such activation involves the accumulation of oxidative stress-generating mitochondria (5), oligomerization of the mitochondrial antiviral signaling protein (9), or sensing of retroviral RNA (48). Thus, pharmacological inactivation of Rab4A may represent a novel, mechanistic target for treatment of SLE.

2. Discovery of mitochondrial dysfunction and activation of the mechanistic target of rapamycin (mTOR) as mediators of pro-inflammatory T-cell development in SLE

We have identified (first) mitochondrial hyperpolarization (MHP) as a novel checkpoint of T cell activation and death (17) and persistent mitochondrial hyperpolarization and increased mitochondrial biogenesis in lupus T cells which are associated with ATP depletion and predisposition to cell death by necrosis (18). The release of necrotic materials is pro-inflammatory in SLE through potent activation of B cells and dendritic cells (19). We discovered (first) that T-cell activation-induced MHP is caused by nitric oxide (NO), which is synthesized by NO synthase isoforms eNOS and nNOS in human T cells (49). Persistent MHP and increased mitochondrial biogenesis are caused by glutathione depletion (18) and enhanced NO production and underlie abnormal T cell activation in SLE (50). Since the mammalian target of rapamycin (mTOR) is a sensor of the Δψm in the outer mitochondrial membrane of T cells, we began to use rapamycin for treatment of SLE patients resistant or intolerant to conventional immunosuppressants (24). Rapamycin effectively controls disease activity in SLE normalizing CD3/CD28-induced calcium fluxing without influencing MHP in lupus T cells (24). This suggested that altered calcium fluxing is downstream or independent of mitochondrial dysfunction. Our most recent studies indicate a role for increased mTOR pathway activity in T cell dysfunction in SLE, by connecting mitochondrial dysfunction to enhanced calcium fluxing and altered formation of the immunological synapse (23). mTOR is a component of two interacting signaling complexes, mTOR complex 1 (mTORC1) and 2 (mTORC2). While mTORC1 is activated (5,20,23), mTORC2 is inhibited in lupus T cells (51). Such skewing may account for depletion of Tregs and expansion of effector T cells that produce IL-4 and IL-17 in SLE patients (22,51). mTORC1 activation contributes to the pathogenesis of SLE and related autoimmune diseases (13). Rapamycin elicits rapid, progressive, and sustained improvement of disease activity via correcting abnormal T-cell lineage specification in patients with active SLE (52). In particular, rapamycin blocked the activity of mTOR complex 1 in all T cells, expanded CD4+CD25+FoxP3+ regulatory, CD4+ central-memory (CD62L+CD197+), and CD8+ effector-memory (CD62L-CD197-) T cells and inhibited the pro-inflammatory necrosis and IL-4 production of CD4-CD8- double-negative T cells after 12 months (52). Unlike effector cells, Tregs of SLE patients exhibit deficient autophagy due to activation of an mTORC1/IL-21 positive feedback loop. Importantly, rapamycin treatment reverses deficient autophagy and facilitates the development and function of Tregs is patients with SLE (53).

The role of mitochondrial dysfunction in pathogenesis of autoimmunity has been supported by linking non-synonymous genetic mutations in mitochondrial DNA to disease susceptibility in patients with SLE and multiple sclerosis (54). The susceptibility gene Sle1c2 was identified by estrogen-related receptor gamma (ESRRG) which is a transcription factor that regulates mitochondrial biogenesis and mediates CD4 T-cell hyper-reactivity in lupus-prone mice (6). Mitochondrial oxidative stress induces oligomerization of the mitochondrial antiviral signaling protein (MAVS) which triggers interferon production in patients with SLE (9).

Comprehensive metabolome analyses revealed an accumulation of pentose phosphate pathway (PPP) metabolites, depletion of cysteine, and the accumulation of kynurenine in lymphocytes of lupus patients relative to matched healthy controls (47). Kynurenine was identified as a metabolic trigger of mTORC1 activation and expansion of DN T cells (47). We are interested to better define the cross-talk between the accumulation of oxidative stress-generating mitochondria and activation of mTOR in human and murine models, including newly developed mice lacking HRES-1/Rab4 and the PPP enzyme, transaldolase.

Dysfunction of mitochondria due to blocked electron transport chain activity (55) and their accumulation due to inhibited mitophagy (5) lead to oxidative stress in lupus T cells (12). In turn, oxidative stress activates mTORC1 (23,56,57) which can be effectively targeted for therapeutic intervention in SLE. We initiated two mechanistic clinical trials which are aimed at blocking the activation of mTOR complex 1 (mTORC1), directly by using rapamycin (22) and indirectly by using the antioxidant, N-acetylcysteine (20). Mitochondrial dysfunction and mTORC1 activation are also detectable in the liver of lupus-prone mice, which has been identified as an early event of disease pathogenesis that triggers the production of antiphospholipid autoantibodies (28). Given that mTOR activation has emerged as a biomarker and central pathway to autoimmune disorders, cancer, obesity and aging, personalized mTOR blockade holds promise to extend life span through preventing and foiling these conditions (58).

3. Discovery of transaldolase and its role in metabolic control of apoptosis, inflammation, autoimmunity, and progressive liver disease

Human transaldolase (TAL) was originally discovered and cloned in our laboratory (14) and identified as a metabolic regulator of programmed cell death via controlling the mitochondrial transmembrane potential (15-17). Expression of transaldolase is controlled by an interplay between the transcription factors ZNF143 and AP2 (59). Transaldolase modulates the tissue-specific activity of the pentose phosphate pathway (27,59). The recently discovered genetic deficiency of transaldolase due to deletion of serin171 causes degradation of the enzyme in the proteasome (60). Transaldolase deficiency influences the pentose phosphate pathway, mitochondrial homeostasis, and apoptosis signal processing in human B cells (61). Transaldolase is cleaved and inactivated by granzyme B that may sensitize target cells to apoptosis induced by cytotoxic T cells (62). We have developed transaldolase-deficient mice that exhibit mitochondrial dysfunction in the sperm and some other cell types. Transaldolase-deficient male mice are infertile due to sperm dysmotility resulting from the loss of the mitochondrial transmembrane potential and diminished ATP production (63). Transaldolase-deficient mice spontaneously develop non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) (26). NASH, cirrhosis, and HCC but not NAFLD are preventable by life-long treatment with N-acetylcysteine (26). These findings are relevant for the pathogenesis of chronic liver disease progressing from NAFLD to NASH, cirrhosis, and HCC in humans since transaldolase deficiency has already been documented in ten children, all with liver disease of varying severity. Mice deficient in transaldolase are also predisposed to acetaminophen/Tylenol-induced liver necrosis (26), the leading cause of acute liver failure in the US. Due to mitochondrial dysfunction and activation of mTORC1, Transaldolase deficiency predisposes to the production of antiphospholipid autoantibodies (28). Transaldolase-deficient mice are also susceptible to other autoimmune inflammatory diseases, which are currently being characterized (64).

4. Clinical research

To test the clinical relevance of our basic research findings, we have begun developing mechanistic clinical trials. We described first that rapamycin may be an effective treatment for lupus. We received investigator-initiated grant support from Wyeth, now Pfizer, to study prospectively the impact of rapamycin on global gene expression and activation of T cells and clinical outcomes in an open-label trial of 40 lupus patients (clinicaltrials.gov: IND No. 101,566). We are currently in discussion with NIAID about a follow-up randomized, placebo-controlled trial with rapamycin in SLE. In addition, mTORC1 blockade with rapamycin may also benefit rheumatic diseases other than SLE (13). Our double-blind placebo-controlled study supported by NIH will determine the effect of NAC on glutathione depletion, mitochondrial hyperpolarization, and calcium signaling in lupus T cells and the clinical outcomes in SLE patients (clinicaltrials.gov: IND No 101,320). The 1st phase of our study double-blind placebo-controlled randomized study shows improved disease activity in NAC-treated SLE patients, relative to placebo, by reversing glutathione depletion and mTORC1 activation in T lymphocytes (20). Within the context of this trial, we also discovered that SLE patients exhibit elevated attention deficit and hyperactivity disorder symptoms that respond to treatment with NAC (21). NAC may be beneficial for other co-morbidities of SLE, such as anti-phospholipid syndrome (65) and liver disease (30). To support the continuation of this study, a clinical trial center grant (UO1) and multicenter planning grant (U34) have been submitted to NIH. A grant award for planning of the multicenter trial has been issued by NIAMS for the period of 8/1/2016-7/31/2018. Application for planning a phase II mechanistic clinical trial to confirm preliminary results (52) is pending.

1. A. Perl, B.  Fekete, P.  Gergely, and A.G.B.  Kovach (1982) Demonstration of Fc and C3b receptors on rat perikarya. Acta Physiol. Hung. 60, 53‑56. PMID: 6223508
2. A. Perl, R.  Gonzalez‑Cabello, I.  Lang, and P. Gergely (1982) Depressed natural and lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells in patients with systemic lupus erythematosus. Immunol. Comm. 11, 431‑440. PMID: 7169224
3. A. Perl, E.  Pocsik, R.  Gonzalez‑Cabello, I.  Lang and P.  Gergely (1983) Human lectin‑dependent T‑cell‑mediated cytotoxicity against HEp‑2 cells. Acta Physiol. Hung. 61, 225‑231. PMID: 6606296
4. A. Perl, R.  Gonzalez‑Cabello, I.  Lang, P. Somos and P. Gergely (1983) Depressed lectin‑dependent cell‑mediated cytotoxicity against  adherent  HEp‑2 cells in patients with carcinoma of the uterine cervix. Cancer. Immunol. Immunother. 15, 155‑158. PMID: 6553513
5. A. Perl, R. Gonzalez‑Cabello, E. Pocsik, I. Lang and P. Gergely (1983) Effect of Fc receptor blocking on human natural and lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Immunol. Letters, 6, 317‑321.  PMID: 6195101
6. A. Perl, R.  Gonzalez‑Cabello and P.  Gergely (1983) Stimulation of lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells by carrageenan. Clin. Exp. Immunol. 54, 567‑572. PMID: 6652971; PMCID: PMC1535892
7. E. Pocsik, R.  Gonzalez‑Cabello, K.  Benedek, A.  Perl, I.  Lang and P.  Gergely (1983) Characterization of the effector cells in Con A‑induced cytotoxicity against HEp‑2 tumour targets. Acta Med. Hung. 40, 41‑46. PMID: 6607455
8. A. Perl, R. Gonzalez‑Cabello, I. Lang and P. Gergely (1984) Effector activity of OKT4+ and OKT8+ T‑cell subsets in lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Cell. Immunol. 84, 185‑193. PMID: 6230158
9. P. Gergely, K.  Nekam, I.  Lang, L.  Kalmar, R.  Gonzalez‑Cabello and A. Perl (1984) Ketoconazole in vitro inhibits mitogen‑induced blastogenesis, antibody‑dependent cellular cytotoxicity, natural killer activity and random migration of human leukocytes. Immunopharmacology, 7, 167‑170. PMID: 6088429
10. A. Perl, R.  Gonzalez‑Cabello and P. Gergely (1984) Depressed effector activity of OKT4+ and   OKT8+ T‑cell subsets in lectin‑dependent cell‑mediated cytotoxicity to  HEp‑2  cells in patients with systemic lupus erythematosus. J. Clin. Lab. Immunol. 15, 95‑100. PMID: 6240539
11. Lang I, Feuer L, Nekam K, Perl A, Szigeti A, Gergely P, Feher J. (1984) Effect of Litoralon therapy on the lymphocytotoxicity in patients with malignant tumors (In Hungarian). Orv. Hetil. 125:2193-2196. PMID: 6472845
12. J. Feher, A.  Cornides, A.  Vereckei, I.  Lang, K. Nekam, A. Perl and P. Gergely (1984) Immunomodulatory effect of new radical scavengers. Drugs Expt. Clin. Res. X(8‑9) 549‑562.
13. K. Nekam, I.  Lang, L.  Kalmar, A. Perl and P.  Gergely (1984) Isoprinosine:  recent experimental and therapeutic results with an antiviral immune modifier. Tissue Cult. Res, 173‑178.
14. A. Perl, R. Gonzalez‑Cabello, K. Benedek, K. Nekam, I. Lang and P. Gergely (1985) Effect of histamin‑receptor blocking on human  natural  and lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Thymus, 7, 111‑118. PMID: 4012822
15. A. Perl, R. Gonzalez‑Cabello, I. Lang and P. Gergely (1985) Depressed lectin‑dependent cell‑mediated cytotoxicity against HEp‑2 cells in patients with different metastatic solid tumors. Acta Physiol. Hung. 65, 149‑153. PMID: 3872553
16. A. Perl, R.  Gonzalez‑Cabello, L.  Falucskai, P.  Gergely, and J. Feher (1985) Contrasting effects of RNA and protein synthesis blocking on natural and lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Experientia, 41, 1344‑1346. PMID: 2412880
17. A. Perl, R.  Gonzalez‑Cabello, K.  Nekam, P.  Gergely and J Feher (1985) Stimulation by thymopoietin oligopeptides of lectin‑dependent cell‑mediated cytotoxicity in patients with systemic lupus erythematosus. J. Clin. Lab. Immunol. 18, 119‑122. PMID: 3910838
18. A. Perl, I.  Lang, R. Gonzalez‑Cabello, J. Filep, K. Nekam, P. Gergely and J Feher (1986) Indomethacin abrogates   the suppression by cyclosporin A of lectin‑dependent cell‑mediated cytotoxicity to HEp‑2 cells. Immunopharmacology, 11, 39‑45. PMID: 3957649
19. A. Perl, R.  Gonzalez‑Cabello, T.  Laskay, M. Benczúr, I. Lang, K. Onody, K. Nekam, P. Gergely and J Feher (1986) Lectin‑dependent cell‑mediated cytotoxicity and blastogenesis by LGL‑enriched and depleted lymphocytes. Clin. Exp. Immunol. 63, 171‑178. PMID: 3955881; PMCID: PMC1577327
20. A. Perl, G. Repassy, R. Gonzalez‑Cabello, I. Lang and P. Gergely (1986) Depressed lectin‑dependent and augmented antibody‑dependent cell‑mediated cytotoxicity in patients with stage I cancer of the larynx. Natural Immunity and Cell Growth Regulation, 5, 100‑106. PMID: 3487714
21. A. Perl, R.  Gonzalez‑Cabello, K.  Onody, I. Bodo and P. Gergely (1986) Independence of depressed lectin‑dependent cell‑mediated cytotoxicity from interleukin‑2 production in patients with systemic lupus erythematosus. Clin. Exp. Immunol. 65, 286‑292. PMID: 3491706
22. A. Perl, A. Szigeti, P. Gergely, J. Feher, E. Magyarosi and M. Sellyei (1986) Abrogation by chemotherapy of T‑cell antigen expression in B‑cell chronic lymphocytic leukemia. N. Engl. J. Med. 314, 186‑187. PMID: 2417119
23. A. Perl, R.J.  Looney, D.H.  Ryan and G.N. Abraham (1986) The low affinity 40 kD Fc‑gamma receptor and the transferrin receptor can be alternative or simultaneous target structures on cells sensitive for natural killing. J. Immunol. 136, 4714‑4720.
24. T. Bakacs, K. Totpal, G. Ringwald, A. Perl and P. Gergely (1986) Quantitative determination of anti‑A‑dependent cytotoxicity of human peripheral blood monocytes. J. Clin. Lab. Immunol. 19, 143‑147.
25. R. Gonzalez‑Cabello, A. Perl,  L.  Kalmar and P. Gergely (1987) Short‑term stimulation of lymphocyte proliferation by indomethacin in vitro and in vivo. Acta Physiol. Hung. 70, 25‑30.
26. J. Feher,  I.  Lang,  Zs.  Pollak,  K.  Nekam,  R.  Gonzalez‑Cabello, A. Perl and P. Gergely (1987)  Immunomodulatory and membrane protective effect of dihydroquinoline type antioxidants. In: Progress in Radio‑Oncology, Ed.: Karcher, K.H., ICRO, Vienna, pp. 218.
27. K. Nekam, A. Perl, P. Gergely, R. Gonzalez‑Cabello and J. Feher (1987) Effect of dialyzable lymphocyte extracts on lectin‑dependent cell-mediated cytotoxicity in vitro. In Proceedings of the Fifth International Symposium on Transfer Factor.  Mayer V. and Borvak J. (Eds.) Bratislava, Czechoslovakia.
28. I.  Lang,  K.  Nekam,  Gy.  Deak,  G.  Muzes,  R.  Gonzalez‑Cabello,  J.  Kadar, A. Perl, P. Gergely and  J.  Feher  (1987)  Effect of  (+)cyanidanol‑3  on cellular immune reactions and on superoxide dismutase activity in vitro. Free Rad. Res. Comm. 4, 51‑60.
29. A. Cornides,  J.  Feher,  A. Perl, P. Gergely and A. Gogl (1987) Metronidazol induced liver injury. Hepatology, 18, 11‑13.
30. A. Perl,  N. Wang, J.M. Williams, M.J. Hunt, S.I. Rosenfeld, J.J. Condemi, C.H. Packman and  G.N.  Abraham  (1987)  Aberrant immunoglobulin and c‑myc gene rearrangements in patients with non‑malignant monoclonal cryoglobulinemia. J. Immunol. 139, 3512‑3520.
31. A. Perl,  P.D.  Gorevic,  D.H.  Ryan,  J.J.  Condemi,  R.J. Ruszkowski and G.N. Abraham
    (1989)  Clonal  B‑cell  expansions  in  patients  with  essential mixed cryoglobulinemia. Clin. Exp. Immunol. 76, 54‑60.
32. A. Perl, J.P. DiVincenzo, P. Gergely, J.J. Condemi and G.N. Abraham (1989) Detection and mapping   of   polymorphic  KpnI  alleles  in  the  human  T‑cell  receptor  constant  beta‑2  locus. Immunology, 67, 135‑138.
33. A. Perl, J.D.  Rosenblatt, I.S.Y.  Chen, J.P. DiVincenzo, R. Bever, B.J. Poiesz, and G.N.
    Abraham (1989)  Detection and  cloning of  new HTLV‑related sequences in man. Nucleic Acids Res., 17, 6841‑6854.
34. A. Perl, J.P.  Divincenzo, D.H. Ryan, P. Gergely, A. Szigeti, J. Feher and G.N. Abraham
    (1990) Rearrangement of the T‑cell receptor alpha, beta and gamma chain genes in B‑cell chronic lymphocytic leukemia. Leukemia Res. 14, 131‑137.
35. G.N. Abraham, A.  Perl, P.D.  Gorevic, J.M.  Williams, G. Jones, and R.A. Kyle (1990)
    Molecular genetic analysis of human monoclonal gammopathies.  In: Biomedical Advances in Aging (Ed. A.L. Goldstein). Plenum Press, New York, pp. 355‑362.
36. Perl A, Feher J. Polymerase chain reaction in clinical diagnosis (In Hungarian). (1990) Orv. Hetil. 131:671-675.
37. Perl, A. (1990) Role of a prostaglandin E1 analogue in prevention of acute graft rejection by cyclosporin A. N. Engl. J. Med., 323, 831‑832.
38. A. Perl, K.  Nagy, T.  Pazmany, C. Isaacs, K. Baraczka, T. Szabo, & J. Feher (1990) No evidence for HTLV‑I or HTLV‑II infection in patients with multiple sclerosis. Arch. Neurol. 47, 1061‑1063.
39. Perl, A., Gorevic, P.D., Condemi,  J.J.,  Papsidero,  L., Poiesz, B.J. and Abraham, G.N.
    (1991) Antibodies to retroviral proteins and reverse transcriptase activity in patients with essential cryoglobulinemia. Arthritis. Rheum. 34, 1313‑1318.
40. Perl, A., Isaacs, C.M., Eddy, R.L., Byers, M.G.,and Shows, T.B. (1991) The human T‑cell
    leukemia virus‑related endogenous sequence (HRES‑1)  is  located  on  chromosome  1  at  q42. Genomics, 11, 1172‑1173.
41. Banki, K., J.S. Maceda, E. Hurley, E. Ablonczy, D. Mattson, L. Szegedy, C. Hung and A.
    Perl (1992) HRES‑1, a human endogenous retroviral sequence encodes a 28 kd protein: a possible autoantigen for HTLV gag‑reactive autoantibodies. Proc. Natl. Acad. Sci. USA, 89, 1939‑1943.
42. Krieg, A.M., Gourley, M.F. and Perl, A. (1992) Endogenous retroviruses: Potential etiologic agents in autoimmunity. FASEB J. 6:2537‑2544.
43. Srivastava, B.I.S., Banki, K. & Perl, A. (1992) Detection of human T‑cell lymphotropic virus type I or  a  related  retrovirus  in  patients  with mycosis fungoides, Sezary syndrome and Kaposi sarcoma. Cancer Res. 52, 4391‑4395.
44. Krieg, A.M., Gourley, M.F., Klinman, D.M., Perl, A., and Steinberg, A.D. (1992)
    Heterogenous expression and induction of human endogenous retroviral sequences in peripheral blood   mononuclear   cells   from patients with   polymyositis and controls.  AIDS Res. Hum. Retrovirus. 12, 1991‑1998.
45. Perl, A. and Banki, K. (1993) Human endogenous retroviral elements and autoimmunity: data and concepts. Trends Microbiol. 1:153‑156.
46. Agarwal, R.K. and Perl, A. (1993) PCR amplification of highly GC‑rich DNA template after denaturation by NaOH. Nucleic Acids Res. 21, 5283‑5284.
47. Banki, K., Halladay, D. and Perl, A. (1994) Cloning and Expression of the Human Gene for Transaldolase: a Novel Highly Repetitive Element Constitutes an Integral Part of the Coding Sequence. J. Biol. Chem. 269:2847‑2851.
48. Banki, K., É.   Ablonczy, M.  Nakamura, and Perl, A.  (1994) Effect of the p40/tax transactivator of human T‑cell lymphotropic virus type I (HTLV‑I) on expression of autoantigens. AIDS Res. Hum. Retrovirus 10:303-308.
49. Magistrelli, C., Halladay, D., Agarwal, R., Ferrante, P., Perl, A. (1994) Mapping and cloning of polymorphic genotypes of the HRES-1 LTR. FASEB J. 8: A4395, manuscript in preparation.
50. Banki, K., E. Colombo, F. Sia, D. Halladay, D. H. Mattson, A.H. Tatum, P. T. Massa, P. E. Phillips, Perl, A. (1994) Oligodendrocyte‑specific expression and autoantigenicity of transaldolase in multiple sclerosis. J. Exp. Med. 180:1649-1663.
51. Perl, A., Colombo, E., Dai, H., Agarwal, R.K., Mark, K., Banki, K., Poiesz, B.J., Phillips, P.E., Hoch, S.O., Reveille, J.D. and Arnett, F.C. (1995). Antibody reactivity to the HRES-1 endogenous retroviral element identifies a subset of patients with systemic lupus erythematosus and overlap syndromes: Correlation with antinuclear antibodies and HLA class II alleles. Arthritis Rheum. 38: 1660-1671.
52. Banki, K. and Perl, A. (1996) Inhibition of the catalytic activity of human transaldolase by antibodies and site-directed mutagenesis. FEBS Lett. 378: 161-165.
53. Banki, K., Hutter, E., Colombo, E., Gonchoroff, N.J. and Perl, A. (1996) Glutathione levels and sensitivity to apoptosis are regulated by changes in transaldolase expression. J. Biol. Chem. 271: 32994-33001.
54. Colombo, E., Banki, K., Tatum, A.H., Daucher, J., Ferrante, P., Murray, R.S., Phillips, P.E. and Perl, A. (1997) Comparative analysis of antibody and cell-mediated autoimmunity to transaldolase and myelin basic protein in patients with multiple sclerosis. J. Clin. Invest. 99:1238-1250.
55. Banki, K., Eddy, R.L., Shows, T.B., Halladay, D.L., Bullrich, F., Croce, C.M., Jurecic, V., Baldini, A. and Perl, A. (1997) The human transaldolase gene is located on chromosome 11 at p15.4-p15.5. Genomics, 45: 233-238.
56. Banki, K., Hutter, E., Gonchoroff, N.J. and Perl, A. (1998) Molecular ordering in HIV-induced apoptosis: oxidative stress, activation of caspases and cell survival are regulated by transaldolase. J. Biol. Chem. 273:11944-11953.
57. Banki, K., Hutter, E., Gonchoroff, N.J. and Perl, A. (1999) Elevation of mitochondrial transmembrane potential and ROI levels are early events and independent from activation of caspases in Fas signaling. J. Immunol. 162:1466-1479. PMID: 9973403; PMCID: PMC4020419
58. Magistrelli, C., Samoilova, E., Agarwal, R.K., Banki, K., Ferrante, P., Vladutiu, A., Phillips, P.E. and Perl, A. (1999) Polymorphic genotypes of the HRES‑1 human endogenous retrovirus locus are associated with systemic lupus erythematosus and autoreactivity. Immunogenetics, 49:829-834.
59. Esposito, M., Venkatesh, V., Otvos, L., Weng, Z., Vajda, S., Banki, K. and Perl, A. (1999) Human transaldolase and cross-reactive viral epitopes identified by autoantibodies of multiple sclerosis patients. J. Immunol. 163:4027-4032.
60. Perl, A. (1999) Mechanisms of viral pathogenesis in rheumatic diseases. Leader. Ann. Rheum. Dis. 58:454-461.
61. Perl, A., Colombo, E., Samoilova, E., Butler, M.C. and Banki. K. (2000) Human transaldolase-associated repetitive elements are transcribed by RNA polymerase III. J. Biol. Chem. 275:7261-7272.
62. Puskas, F., Gergely, P. Jr., Banki, K. And Perl. A (2000) Stimulation of the pentose phosphate pathway and glutathione levels by dehydroascorbate, the oxidized form of vitamin C. FASEB J. 14: 1352-1361.
63. Thorell, S, Gergely, P.Jr., Banki, K. , Perl, A., Schneider, G. (2000) The three-dimensional structure of human transaldolase. FEBS Lett. 475:205-208.
64. Perl, A., Banki, K. (2000) Genetic and metabolic control of the mitochondrial transmembrane potential and reactive oxygen intermediate production in HIV disease. Invited review. Antiox. Redox Signal., 2:551-573.
65. Perl, A. (2001) Editorial. Endogenous Retroviruses in Pathogenesis of Autoimmunity. J. Rheumatol. 28:461-464.
66. Lachaise, F., Martin, G., Drougard, C., Perl, A, Vuillaume, M., Wegnez, M., Sarasin, A., Daya-Grosjean, L. (2001) Relationship between post-translational modification of transaldolase and catalase deficiency in UV-sensitive repair-deficient Xeroderma pigmentosum fibroblasts and SV40-transformed human cells. Free Rad. Biol. Med. 30:1365-1373.
67. Perl, A. (2001) Abnormal Apoptosis in Systemic Lupus. Lupus News, 21:16-17.
68. Gergely, P. Jr., Grossman, C., Niland, B., Puskas, F., Neupane, H., Allam, F., Banki, K., Phillips, P.E. and Perl, A. (2002) Mitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosus. Arthritis Rheum. 46:175-190. PMID: 1181758911817589; PMCID: PMC4020417
69. Puskas, F., Gergely, P., Niland, B., Banki, K. and Perl, A. (2002) Differential regulation of hydrogen peroxide and Fas-dependent apoptosis pathways by dehydroascorbate, the oxidized form of vitamin C. Antiox. Redox Signal. 4:357-369.
70. Perl, A, Gergely, P., Puskas, F. and Banki, K. (2002) Metabolic switches of T cell activation and apoptosis. Antiox. Redox Signal. 4:427-443.
71. Kammer, G.M., Perl, A., Richardson, B.C., Tsokos, G.C. (2002) Abnormal T cell signal transduction in systemic lupus erythematosus. Arthritis Rheum. 46:1139-1154.
72. Gergely, P. Jr., Niland, B., Gonchoroff, N., Pullmann, R. Jr., Phillips, P.E. and Perl, A.(2002) Persistent mitochondrial hyperpolarization, increased reactive oxygen intermediate production, and cytoplasmic alkalinization characterize altered IL-10 signaling in patients with systemic lupus erythematosus. J. Immunol. 169:1092-1101.
73. Nagy, Gy, Koncz, A. and Perl A (2003) T cell activation-induced mitochondrial hyperpolarization is mediated by Ca2+- and redox-dependent production of nitric oxide. J. Immunol. 171:5188-5197.
74. Mukhopadhyay, S., Mousa, S., George, B.R. and Perl, A. (2004) Palpable purpura, polyarthritis, and abdominal pain. Med. J. Aust. 180:121-122.
75. Perl, A., Gergely, P. Jr., Nagy, G., Koncz, A., and Banki, K. (2004). Mitochondrial hyperpolarization: a checkpoint of T-cell life, death, and autoimmunity. Trends Immunol. 25:360-367.
76. Grossman, C. E., Qian, Y., Banki, K., Perl, A. (2004) ZNF143 mediates basal and tissue-specific expression of human transaldolase. J. Biol. Chem. 279: 12190-12205.
77. Perl,A.; Gergely,P.,Jr.; Banki,K. (2004) Mitochondrial dysfunction in T cells of patients with systemic lupus erythematosus. Int. Rev. Immunol. 23:293-313.
78. Grossman, C. E., Niland, B., Stancato, C, Verhoeven, N.M., van der Knaap, M.S., Jakobs, C., Brown, L.M., Vajda, S., Banki, K. and Perl, A. (2004) Deletion of serine 171 causes inactivation, proteasome-mediated degradation and complete deficiency of human transaldolase. Biochem. J. 382:725-231.
79. Nagy, Gy, Barcza. M., Gonchoroff, N., Phillips, P.E. and Perl, A. (2004) Nitric oxide-dependent mitochondrial biogenesis generates Ca2+ signaling profile of lupus T cells. J. Immunol. 173:3676-3683. PMID: 15356113; PMCID: PMC4034140
80. Nagy, Gy, Koncz, A, Phillips, P.E. and Perl, A. (2005) Mitochondrial signal transduction abnormalities in systemic lupus erythematosus. Curr. Immunol. Rev. 1: 61-67.
81. Gergely. P. Jr, Pullmann, R., Stancato, C., Otvos, L. Jr, Koncz, A., Blazsek, A., Poor, Gy, Brown, K.E., Phillips, P.E. and Andras Perl. (2005) Increased prevalence of transfusion-transmitted virus and cross-reactivity with immunodominant epitopes of the HRES-1/p28 endogenous retroviral autoantigen in patients with systemic lupus erythematosus. Clin. Immunol. 116: 124-134.
82. Nagy, Gy, Koncz, A, and Perl, A. (2005) T- and B-cell abnormalities in systemic lupus erythematosus. Crit. Rev. Immunol. 25: 123-140.
83. Nagy, Gy, Koncz, A, and Perl, A. (2005) Signal transduction abnormalities in systemic lupus erythematosus (In Hungarian). Orv. Hetil. 146:1625-1630.
84. Niland, B., Banki, K., Biddison, W.E. and Perl, A. (2005) CD8+ T cell-mediated HLA-A*0201-restricted cytotoxicity to transaldolase peptide 168-176 in patients with multiple sclerosis. J. Immunol. 175: 8365-8378.
85. Quintero M, Mirza N, Chang H, Perl A. (2006) Antiphospholipid antibody syndrome associated with primary angiitis of the central nervous system: report of two biopsy-proven cases. Ann. Rheum. Dis. 65 :408‑9
86. Nagy G. and Perl, A. (2006) The role of nitric oxide in abnormal T cell signal transduction in systemic lupus erythematosus. Clin. Immunol. 118: 145-151.
87. Vas, Gy., Conkrite, K., Amidon, W., Qian, Y., Banki, K., and Perl, A. (2006) Study of transaldolase deficiency in urine samples by LC-MS/MS. J. Mass. Spec. 41: 463-469.
88. Fernandez, D., Bonilla, E., Mirza, N, Niland, B. and Perl, A. (2006) Rapamycin reduces disease activity and normalizes T-cell activation-induced calcium fluxing in patients with systemic lupus erythematosus. Arthritis Rheum. 54: 2983-2988. PMID:16947529; PMCID: PMC4034146
89. Perl, A., Qian, Y, Chohan, K.R., Shirley, C.R., Amidon, W., Banerjee, S., Middleton, F.A., Conkrite, K.L., Barcza, M., Gonchoroff, N., Suarez, S.S., and Banki, K. (2006) Transaldolase is essential for maintenance of the mitochondrial transmembrane potential and fertility of spermatozoa. Proc. Natl. Acad. Sci. USA, 103: 14813-14818. PMID:17003133; PMCID: PMC1595434
90. Nagy, G., Ward, J., Mosser, D.D., Koncz, A., Gergely, P. Jr., Stancato, S., Qian, Y, Fernandez, D., Niland, B., Grossman, C.E., Telarico, T, Banki, K, Perl, A. (2006) Regulation of CD4 expression via recycling by HRES‑1/RAB4 controls susceptibility to HIV infection. J. Biol. Chem. 281: 34574-34591. PMID:16935861
91. Fernandez, D., Bonilla, E., Phillips, P.E. and Perl, A. (2006) Signaling abnormalities in systemic lupus erythematosus as potential drug targets. Endocrin, Metabolic & Immune Disorders – Drug Targets. 6: 305-311.
92. Gergely, P., Perl, A. and Poor, Gy. (2006) Possible pathogenic nature of the recently discovered TT virus. Does it play a role in autoimmune rheumatic diseases? Autoimmun. Rev. 6:5-9.
93. LaRocca, D., Lehmann, D.F., Perl, A., Ozawa, T., Holohan, P. D. (2006) The combination of nuclear and mitochondrial mutations as a risk factor for idiosyncratic toxicity. Brit. J. Clin. Pharm. 63:249-251.
94. Silberstein, M., Landon, M.R., Wang, Y.E., Perl, A. and Vajda, S. (2006) Computational methods for functional site identification suggest a substrate access channel in transaldolase. Genome Inform. 17: 13-22.
95. Koros, A., Hanczko, R., Jambor, Qian, Y., Perl, A. and Molnar-Perl, I. (2007) Analysis of amino acids and biogenic amines in biological tissues as their o-phthalaldehyde/ethanethiol/fluorenylmethyl chloroformate derivatives by high-performance liquid chromatography: A deproteinization study. J. Chromatogr. A 1149: 46-55.
96. Nagy, G., Koncz, A., Fernandez, D. and Perl A. (2007). Nitric oxide, mitochondrial hyperpolarization, and T-cell activation. Free Radic. Biol. Med. 42: 1625-1631.
97. Perl, A. (2007) The pathogenesis of transaldolase deficiency. IUBMB Life 59: 365-373.
98. Bonilla, E., Francis, L., Allam, F., Ogrinc, M., Neupane, H., Phillips, P.E., and Perl, A. (2007) Immunofluorescence microscopy is superior to fluorescent beads for detection of antinuclear antibody reactivity in systemic lupus erythematosus patients. Clin. Immunol. 124:18-21.
99. Hanczko, R., Jambor, A., Perl, A., and I Molnar-Perl (2007) Advances in the o-phthalaldehyde derivatizations: Comeback to the o-phthalaldehyde-ethanethiol reagent. J. Chromatogr. A 1163: 25-42.
100. Bonilla, E., Lee, Y.Y., Phillips, P.E., and Perl, A. (2007) Hypoglycaemia after initiation of etanercept treatment in a patient with type 2 diabetes mellitus. Ann. Rheum. Dis. 66:1688.
101. Pullmann, R. Jr., Bonilla, E., Phillips, P.E., Middleton, F.A. and Perl, A. (2008) Haplotypes of the HRES-1 endogenous retrovirus are associated with development and disease manifestations of systemic lupus erythematosus. Arthritis Rheum. 58: 532-540. PMID: 18240231
102. Francis L, Bonilla E, Soforo E, Neupane H, Nakhla H, Fuller C, and Perl A. (2008) Fatal toxic myopathy attributed to propofol, methylprednisolone, and cyclosporine after prior exposure to colchicine and simvastatin. Clin. Rheumatol. 27:129-31.
103. Perl, A., Nagy, G., Koncz, A., Gergely, P., Fernandez, D., Doherty, E., Telarico, T., Bonilla, E. and Phillips, P.E. (2008) Molecular mimicry and immunomodulation by the HRES-1 endogenous retrovirus in SLE. Autoimmunity, 41:287-297. PMID: 18432409PMID:18432409 DOI: 10.1080/08916930802024764
104. Qian, Y., Banerjee, S., Grossman, C.E., Amidon, A., Nagy, Gy., Barcza, M., Niland, B., Karp, D.R., Banki, K., and Perl, A. (2008) Transaldolase deficiency influences the pentose phosphate pathway, mitochondrial homeostasis, and apoptosis signal processing. Biochem. J. 415:123-134.
105. Vyshkina, T., Sylvester, A., Sadiq, S., Bonilla, E., Canter, J., Perl, A. and Kalman, B.(2008) Association of Common Mitochondrial DNA Variants with Multiple Sclerosis and Systemic Lupus Erythematosus. Clin. Immunol. 129:31-35.
106. Vyshkina, T., Sylvester, A., Sadiq, S., Bonilla, E., Perl, A. and Kalman, B. (2008) CCL genes in multiple sclerosis and systemic lupus erythematosus. J. Neuroimmunol. 200:145-152.
107. Perl, A. (2009) Overview of Signal Processing by the Immune System in SLE. Autoimmun. Rev. 8:177-178.
108. Fernandez D.R. and Perl, A. (2009) Metabolic control of T-cell activation and death in SLE. Autoimmun. Rev. 8:184-189.
109. Fernandez, D.R. Telarico, T., Bonilla, E., Li, Q., Banerjee, S., Middleton, F.A., Phillips, P.E., Crow, M.K., Oess, S., Muller-Esterl, W., and Perl, A. (2009) Activation of mTOR controls the loss of TCRζ in lupus T cells through HRES-1/Rab4-regulated lysosomal degradation. J. Immunol. 182: 2063-2073. PMID:19201859; PMCID: PMC2676112
110. Hanczko, R., Fernandez, D.R., Doherty, E., Qian, Y., Vas, G., Niland, B., Telarico, T., Garba, A., Banerjee, S., Middleton, F.A., Barrett, D., Barcza, M., Banki, K., Landas, S.K. and Perl, A. (2009) Prevention of hepatocarcinogenesis and increased susceptibility to acetaminophen-induced liver failure in transaldolase-deficient mice by N-acetylcysteine. J. Clin. Invest. 119:1546-1557. PMID: 19436114; PMCID: PMC2689120
111. Francis, L. and Perl. A. (2009) Pharmacotherapy of SLE. Expert Opin. Pharmacother. 10: 1481-1494.
112. Perl, A., Fernandez, D., Telarico, T., Francis, L. and Phillips, P.E. (2009) T- and B-cell signaling biomarkers and treatment targets in lupus. Curr. Opin. Rheumatol. 21: 454-464.
113. Perl, A. (2009) Editorial: Emerging New Pathways of Pathogenesis and Targets for Treatment in Systemic Lupus Erythematosus and Sjogren’s Syndrome. Curr. Opin. Rheumatol. 21: 443-447.
114. Bedoya, F., Medveczky, M.M., Lund, T.C., Perl, A., Horvath, J., Jett, S.D. and Medveczky, P.G. (2009) Identification of Mitochondrial Genome Concatamers in AIDS-associated lymphomas and lymphoid cell lines. Leuk. Res. 33:1499-1504.
115. Tily, HI and Perl, A. (2009) Lymphedema: a paradoxical effect of tumor necrosis factor inhibitors – case report and review of literature. BMJ Case Reports [doi:10.1136/bcr.07.2008.0520]
116. Blank, M., Shoenfeld, Y. and Perl, A. (2009) Cross-talk of the environment with the host genome and the immune system through endogenous retroviruses in systemic lupus erythematosus. Lupus, 18: 1136-1143.
117. Soforo, E., Baumgartner, M., Francis, L., Allam, F., Phillips, P.E., and Perl, A. (2010) Induction of systemic lupus erythematosus with TNF blockers. J. Rheumatol. 37:204-205.
118. Francis, L. and Perl. A. (2010) Infection in systemic lupus erythematosus: friend or foe? Int. J. Clin. Rheumatol. 5:59-74.
119. Perl, A. (2010) Editorial: Pathogenic Mechanisms in Systemic Lupus Erythematosus. Autoimmunity, 43:1-6.
120. Perl, A. (2010) Systems biology of lupus: mapping the impact of genomic and environmental factors on gene expression signatures, cellular signaling, metabolic pathways, hormonal and cytokine imbalance and selecting targets for treatment. Autoimmunity 43: 32-47.
121. Tily, H., Banki, K., Hoffman, G.S. and Perl. A. (2010) Detection of lupus anti-coagulant and successful anti-coagulation in familial Sneddon syndrome. Ann. Rheum. Dis. 69: 775-776.
122. Niland, B, Miklossy, G, Banki, K, Biddison, W.E., Casciola-Rosen, L., Rosen, A., Martinvalet, D., Lieberman, J., and Perl, A. (2010) Cleavage of transaldolase by granzyme B causes the loss of enzymatic activity with retention of antigenicity for multiple sclerosis patients. J. Immunol., 184:4025-32.
123. Perl, A., Fernandez, D., Telarico, T, and Phillips P.E. (2010). Endogenous retroviral pathogenesis in lupus. Curr. Opin. Rheumatol. 22:483-492.
124. Nagy, G., Koncz, A., Telarico, T., Fernandez, D., Ersek, B., Buzas, E., and Perl, A. (2010) Central role of nitric oxide in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus. Arth. Res. Ther. 12: N. (http://arthritis-research.com/content/12/3/N)
125. Engelke, Udo F.H., Fokje S.M. Zijlstra, Fanny Mochel, Vassili Valayannopoulos, Daniel Rabier, Leo A.J. Kluijtmans, Andras Perl, Nanda Verhoeven-Duif, Pascale de Lonlay-Debeney, Mirjam M. Wamelink, Cornelis Jakobs, Éva Morava, Ron A. Wevers. (2010) Erythronic Acid as a Novel Biomarker in Transaldolase Deficiency. Biochim. Biophys. Acta – Molecular Basis of Disease. 1802 (11):1028-1035.
126. Fernandez, D. and Perl, A. (2010) mTOR Signaling: A Central Pathway to Pathogenesis in Systemic Lupus Erythematosus? Discov. Med. 9:173-178.
127. Hernández-Negrete, I, Sala-Newby, G.B., Perl, A, Kunkel, G.R., Newby, A.C. and Bond, M. (2011) Adhesion-dependent SKP2 transcription requires selenocysteine tRNA gene transcription activating factor (STAF). Biochem. J. 436:133-143.
128. Perl, A. (2011) Deleterious effects of TNF blockade in SLE. J. Rheumatol. 38:1217.
129. Perl, A., Hanczko, R., Telarico, T., Oaks, Z. and Landas S. (2011). Control of oxidative stress, inflammation, and carcinogenesis through the pentose phosphate pathway by transaldolase. Trends Mol. Med. 17: 395-403. PMID: 21376665
130. Sreih, A., Ezzeddine, R., Leng, L., Lachance, A., Yu, G., Mizue, Y., Pons-Estel, B., Abelson, A-K., Gunnarsson, I., Svenungsson, E., Cavett, J., Glenn, S., Zhang, L., Montgomery, R., Perl, A., Salmon, J., Alarcon-Riquelme, M., Harley, J.B., Bucala, R. (2011) Dual Effect of Macrophage Migration Inhibitory Factor Gene on the Development and the Severity of Human Systemic Lupus Erythematosus. Arthritis Rheum. 63: 3942-3951.
131. Talaber, G. and Perl, A. (2011) SLE: a Metabolic Disease of T Cells? OMICS Rheumatology 1:e103. http://dx.doi.org/10.4172/2161-1149.1000e103
132. Talaber G, Perl A (2012) The molecular pathogenesis of SLE. Immunolologia Szemle (Immunological Quarterly, Hungarian with English abstract) 1:4-11
133. Perl, A. (2012) Editorial. Oxidative stress and endosome recycling are complementary mechanisms reorganizing the T-cell receptor signaling complex in SLE. Clin. Immunol. 142: 219-222.
134. Perry, D.J., Yin, Y, Telarico, T., Baker, H.V., Dozmorov, I, Perl, A. and Morel, L. (2012) Murine Lupus Susceptibility Locus Sle1c2 Mediates CD4+ T cell Activation and Maps to Estrogen-Related Receptor Gamma Esrrg. J. Immunol. 189: 793-803. PMID: 22711888 22711888; PMCID: PMC3392454
135. Caza, T.N., Talaber, G. and Perl, A. (2012) Metabolic regulation of organelle homeostasis in lupus T cells. Clin. Immunol. 144: 200-213. PMID: 22836085
136. Meszaros, Z., Perl, A, Faraone, S. (2012) Psychiatric symptoms in systemic lupus erythemathosus. J. Clin. Psych. 73: 993-1001. PMID:22687742
137. Lai, Z-W, Hanczko, R., Bonilla, E, Caza, T.N., Clair, B., Bartos, A., Miklossy, G, Jimah, J., Doherty, E, Tily, H., Francis, L, Garcia, R., Dawood, M., Yu, J., Ramos, I., Coman, I., Faraone, S.V., Phillips, P.E. and Perl, A. (2012). N-acetylcysteine reduces disease activity by blocking mTOR in T cells of lupus patients. Arthritis Rheum. 64: 2937-2946. PMID: 22549432; PMCID: PMC3411859
138. Alessandri, C, Barbati, C., Vacirca, D., Piscopo, P., Confaloni, A.M., Maselli, A., Colasanti, T., Conti, F., Truglia, S., Perl, A., Valesini, G, Ortona, E., Malorni, W, and Pierdominici, M. (2012) T lymphocytes from patients with Systemic Lupus Erythematosus are resistant to induction of autophagy. FASEB J. 26: 4722-4732. PMID: 22835828; PMCID: PMC3475261
139. Garcia, R.J., Francis, L., Dawood, M, Lai, Z-W., Faraone, S.V., and Perl, A. (2013) Attention Deficit and Hyperactivity Disorder Scores are Elevated and Respond to NAC treatment in patients with SLE. Arthritis Rheum. 65: 1313-1318. PMID: 23400548
140. Singh N, Birkenbach M, Caza T, Perl A, Cohen PL. (2013) Tuberous sclerosis and fulminant lupus in a young woman. J. Clin. Rheumatol. 19(3):134-7. doi: 10.1097/RHU.0b013e318289c033. PMID: 23519178
141. Gilkeson GS, Mashmoushi AK, Ruiz P, Caza TN, Perl A, and Oates JC. (2013) Endothelial Nitric Oxide Synthase Reduces Crescentic and Necrotic Glomerular Lesions, Reactive Oxygen Production, and MCP1 Production in Murine Lupus Nephritis. PLoS ONE 8(5): e64650. doi:10.1371/journal.pone.0064650 PMID: 23741359
142. Lai, Z-W, Borsuk, R., Shadakshari, A., Yu, J., Dawood, M., Garcia, R., Francis, F., Tily, H., Bartos, A., Faraone, S.V., Phillips, P.E. and Perl. A. (2013). mTOR activation triggers IL-4 production and necrotic death of double-negative T cells in patients with systemic lupus eryhthematosus. J. Immunol. 191: 2236-2246. doi: 10.4049/jimmunol.1301005. PMID: 23913957
143. Perl, A. (2013) Oxidative stress in the pathology and treatment of systemic lupus erythematosus. Nat. Rev. Rheumatol. 9:674-686. PMID: 24100461
144. Caza, T.N., Fernandez, D.R., Talaber, G., Oaks, Z., Haas, M., Madaio, M.P., Lai, Z-W, Miklossy, G., Singh, R.R., Chudakov, D.M., Malorni, W., Middleton, F., Banki, K, and Perl, A. (2014) HRES-1/RAB4-mediated depletion of Drp1 impairs mitochondrial homeostasis and represents a target for treatment in SLE. Ann. Rheum. Dis. 73:1888-1897. PMID:23897774; PMCID:PMC4047212
145. Oaks, Z. and Perl, A. (2014). Metabolic control of the epigenome in systemic lupus erythematosus. Autoimmunity, 47:256-264. PMCID: PMC4034124
146. Fali, T, Le Dantec, C, Thabet, Y., Jousse, S., Hanrotel, C., Brooks, W.H., Perl, A., and Renaudineau, Y. (2014) DNA methylation modulates HRES1/p28 expression in B cells from patients with lupus. Autoimmunity, 47:265-271. PMID: 24117194; PMCID: PMC4034120
147. Talaber, G., Miklossy, G., Oaks, Z, Liu, Y, Tooze, S.A., Chudakov, D.M., Banki, K. and Perl. A (2014) HRES-1/Rab4 promotes the formation of LC3+ autophagosomes and the accumulation of mitochondria during autophagy. PLoS ONE, 9(1): e84392.
148. Caza, T., Oaks, Z and Perl, A. (2014) Interplay of infections, autoimmunity, and immunosuppression in systemic lupus erythematosus. Int. Rev. Immunol. 33(4):330-363.
149. Doherty, E, Oaks, Z. and Perl, A. (2014) Increased Mitochondrial Electron Transport Chain Activity at Complex I is Regulated by N-acetylcysteine in Lymphocytes of Patients with Systemic Lupus Erythematosus. Antioxid. Redox Signal. 21: 56-65. PMID: 24673154;
150. Kato, H. and Perl, A. (2014) Mechanistic Target of Rapamycin Complex 1 Expands Th17 and IL-4+ CD4-CD8- Double-Negative T Cells and Contracts Regulatory T Cells in Systemic Lupus Erythematosus. J. Immunol. 192:4134-4144; PMID: 24683191. PMCID: PMC3995867.
151. Oaks Z and Perl A. TALDO1 (transaldolase 1). Atlas Genet Cytogenet Oncol Haematol. Feb 2014; 18(2).
152. Lai, Z-W, Marchena-Mendez, I. and Perl, A. (2015) Oxidative stress and Treg depletion in lupus patients with anti-phospholipid syndrome. Clin. Immunol. 158:148-152. PMID: 26366134; PMCID:PMC4464983
153. Perl, A. (2015) mTOR Activation is a Biomarker and Central Pathway to Autoimmune Disorders, Cancer, Obesity, and Aging. Ann. NY Acad. Sci. 1346:33-44. PMID: 25907074; PMCID: PMC4480196
154. Liu, Y., Yu, J., Oaks, Z., Marchena-Mendez, I., Francis, L., Bonilla, E., Aleksiejuk, P., Patel, J, Banki, K., Landas, S.K. and Perl, A. (2015) Liver injury correlates with biomarkers of autoimmunity and disease activity and represents an organ system involvement in patients with systemic lupus erythematosus. Clin. Immunol. 160:319-327. PMID: 26366134; PMCID:PMC4583603
155. Perl, A., Hanczko, R., Lai, Z-W, Oaks, Z., Kelly, R., Borsuk, R., Asara, J.M., and Phillips, P.E. (2015) Comprehensive metabolome analyses reveal N-acetylcysteine-responsive accumulation of kynurenine in systemic lupus erythematosus: implications for activation of the mechanistic target of rapamycin. Metabolomics. 11:1157-1174. PMID: 26366134; PMCID: PMC4559110
156. Joseph, N., Zhang-James, Y., Perl, A., and Faraone, S.V. (2015) Oxidative Stress and Attention Deficit Hyperactivity Disorder: A Meta-Analysis. J. Atten. Disord. 19:915-924. PMID: 24232168; PMCID: PMC5293138
157. Perl, A. (2016). Mechanistic Target of Rapamycin Pathway Activation in Rheumatic Diseases. Nat. Rev. Rheumatol. 12:169-182. PMID: 24232168; PMCID: PMC5314913
158. Klionsky, D.H…Perl, A… (2016) Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy. Autophagy. 12: 1-122. PMID: 24232168 PMCID:PMC4835977 [Available on 2017-01-21]
159. Oaks, Z., Winans, T, Caza, T., Fernandez, D., Liu, Y, Landas, S.K, Banki, K. and Perl, A. (2016) Mitochondrial dysfunction in the liver and antiphospholipid antibody production precede disease onset and respond to rapamycin in lupus-prone mice. Arthritis Rheumatol. (Featured In This Issue). 68(11):2728-2739. PMID: 27332042; PMCID:PMC5083168
160. Perl, Al. (2016) LINEing Up to Boost Interferon Production: Activation of Endogenous Retroviral DNA in Autoimmunity. Arthritis Rheumatol. Invited Editorial. 68:2568-2570. PMID: 27338170; PMCID: PMC5083194
161. Buskiewicz, I.A., Montgomery, T., Yasewicz, E.C., Huber, S.A., Murphy, M.P., Hartley, R.C., Kelly, R., Crow, M.K., Perl, A, Budd, R.C. and Koenig, A. (2016) Reactive oxygen species induce virus-independent MAVS-oligomerization in systemic lupus erythematosus. Sci. Signal. Vol. 9, Issue 456, pp. ra115 DOI: 10.1126/scisignal.aaf1933. PMID: 27899525; PMCID: PMC5321043
162. Perl, A., Lai, Z, Oaks, Z., Asara, A., Hanczko, R., Kelly, R., and Phillips, P. (2016).
     Metabolome checkpoints of mTOR activation and clinical responsiveness in SLE. Lupus Sci. Med. (Suppl.1) A14-A15. http://dx.doi.org/10.1136/lupus-2016-000179.29
163. Oaks, Z, Winans, T, Huang, N, Banki, K. and Perl, A. (2016) Activation of the mechanistic target of rapamycin in SLE: Explosion of evidence in the last five years. Curr. Rheum. Rep. Dec;18(12):73. PMID.PMID: 27812954; DOI:10.1007/s11926-016-0622-8
164. Bonilla E, Shadakshari A, Perl A. (2016) Association of psoriasis and psoriatic arthritis with systemic lupus erythematosus. Rheumatol. Orthop. Med. https://oatext.com/pdf/ROM-1-105.pdf; DOI: 10.15761/ROM.1000105.
165. Doherty, E. and Perl, A. (2017) Measurement of Mitochondrial Mass by Flow Cytometry during Oxidative Stress. React. Oxyg. Species, 4 (10): 275-283. ISSN 2380-2367. PMID: 29806036; PMCID: PMC5964986
166. Perl, A. (2017) Metabolic control of immune system activation in rheumatic diseases. Arthritis Rheumatol. 69:2259-2270. PMID: 28841779 PMCID: PMC5711528 [Available on 2018-12-01]
167. Kato, H. and Perl, A. (2018) The IL-21-mTOR axis blocks differentiation and function of regulatory T cells of systemic lupus erythematosus patients by suppression of autophagy. Arthritis Rheumatol. 70(3):427-438. PMID: 29161463; PMCID: PMC5826851
168. Lai, Z, Kelly, R., Winans, T., Marchena, I., Shadakshari, A., Yu, J., Dawood, M., Garcia, R., Tily, H. Francis, L., Faraone, S.V ., Phillips, P.E. and Perl, A. (2018) Sirolimus in patients with clinically active systemic lupus erythematosus resistant to, or intolerant of, conventional medications: a single-arm, open-label, phase 1/2 trial. Lancet, 391:1186-1196. PMID: 29551338; PMCID: PMC5891154
169. Huang, N. and Perl, A. (2018) Metabolism as a target for modulation in autoimmune diseases. Trends Immunol. 39:562-576. PMID: 29739666;
170. Minchenberg SB, Chaparala G, Oaks Z, Banki K, and Perl A (2018) Systemic lupus erythematosus-myasthenia gravis overlap syndrome: Presentation and treatment depend on prior thymectomy. Clin. Immunol. 194:100-104. PMID: 30025818; PMC6089637.
171. Perl, A., Lai, Z, Kelly, R., Faraone, S.V., and Phillips, P.E. (2018) Sirolimus for systemic lupus erythematosus – Authors’ reply. Lancet, 392:734. PMID: 30191826;
172. Zhi-Wei Lai, Ryan Kelly, Thomas Winans, Ivan Marchena, Ashwini Shadakshari, Julie Yu, Maha Dawood, Ricardo Garcia, Hajra Tily, Lisa Francis, Stephen V Faraone, Paul E Phillips and Andras Perl (2018) Blockade of the mechanistic target of rapamycin elicits rapid and lasting improvement of disease activity through restraining pro-inflammatory T cell lineage specification in patients with active SLE. Lupus Sci. Med. Aug 2018, 5 (Suppl 2) A13-A14; DOI: 10.1136/lupus-2018-lsm.26
173. Perl, A. (2018) mTOR-Dependent Autophagy Contributes to End-Organ Resistance and Serves as Target for Treatment in Autoimmune Disease. EBioMedicine, 36:12-13; PMID: 30262258; PMC6197622; DOI: 10.1016/j.ebiom.2018.09.033
174. Budd, R., Perl, A., Blanco, L., Kaplan, M. J., Buskiewicz, I., Fortner, K. (2018) Redox-driven type I interferon in SLE and its treatment with MitoQ. Lupus Sci. Med. 6 (Suppl. 1) A28-A29; http://dx.doi.org/10.1136/lupus-2019-lsm.38
175. Liu, E. and Perl, A. (2019) Pathogenesis and treatment of autoimmune rheumatic diseases. Curr. Opin. Rheum. 31: 307-315. PMID: 30920455; PMCID: PMC6447054 [Available on 2020-05-01]
176. Oaks, Z., Jimah. J., Grossman, C.C., Beckford, M., Kelly, R., Banerjee, S., Niland, B., Miklossy, G., Kuloglu, Z., Kansu, A., Lee, W., Szonyi, L., Banki, K. and Perl, A., (2020) Transaldolase haploinsufficiency in subjects with acetaminophen-induced liver failure. J. Inherit. Metab. Dis. 43: 496-506. PMID: 31769880
177. Godavarthy, A., Kelly, R, Jimah, J., Beckford, M., Caza, T., Fernandez, D.R., Huang, N., Duarte, M., Lewis, J., Fadel, H.J., Poeschla, E.M., Banki, K. and Perl, A., (2020) Lupus-associated endogenous retroviral LTR polymorphism and epigenetic imprinting promote HRES-1/Rab4 expression and mTOR activation. JCI Insight, 5: e134010. PMID:31805010
178. Wyman, B. and Perl, A. (2020) Metabolic pathways mediate pathogenesis and offer targets for treatment in rheumatic diseases. Curr. Opin. Rheum. 32:184-191. PMID:31895126
179. Greca, I., Ben Gabr, J., Perl, A., Bryant, S. and Zaccarini, D. (2020) Trauma Induced Calcium Pyrophosphate Deposition Disease of the Lumbar Spine. Case Rep. Rheumatol. https://doi.org/10.1155/2020/3218350; PMID: 32095306;
180. Fortner K.A., Blanco, L.P., Buskiewicz, I., Huang, N., Gibson, P.C., Cook, D.L., Yuen, P.S.T., Murphy, M.P., Perl, A, Kaplan,, M.J., Budd, R.C (2020) Targeting Mitochondrial Oxidative Stress with MitoQ Reduces NET Formation and Kidney Disease in Lupus-Prone MRL-lpr Mice. Lupus Sci. Med. PMID: 32343673; PMCID: PMC7199895; doi: 10.1136/lupus-2020-000387
181. Dziamski, K., Sharmeen, S., Banki, K., and Perl, A. (2020) Nine-test panel has superior sensitivity to detect antiphospholipid antibody syndrome in patients with or without SLE. Clin. Immunol. In press. PMID: 32200114; PMCID: PMC7200285 (available on 2021-05-01); DOI: 10.1016/j.clim.2020.108388
182. Piranavan, P., Bhamra, M. and Perl, A. (2020). Metabolic targets for treatment of autoimmune diseases. Immunometabolomics, 2020; 2(2): e200012. doi: 10.20900/immunometab20200012. PMID: 32341806; PMCID: PMC7184931
183. Piranavan, P. and Perl, A. (2020). Management of cardiovascular disease in patients with systemic lupus erythematosus. Expert Opin. Pharmacother. 21:1617-1628. PMID: 32511034;
184. Ben Gabr, J., Liu, E., Mian, S., Pillittere, J., Bonilla, E., Banki, K., Perl, A (2020) Successful treatment of secondary macrophage activation syndrome with emapalumab in a patient with newly diagnosed adult-onset Still’s disease: case report and review of the literature. Ann. Transl. Med. 2020 Jul;8(14):887. doi: 10.21037/atm-20-3127. PMID: 32793731; PMCID: PMC7396773.
185. Ben Gabr, J., Bilal, H., Mirchia, K. and Perl, A (2020) The Use of Eculizumab in Tacrolimus-Induced Thrombotic Microangiopathy. J. Investig. Med. High Impact Case Rep. 8:2324709620947266; PMID: 32757799; PMCID: PMC7412890
186. Ibrahim, H, Perl, A., Smith, D., Lewis, T., Kon, Z., Goldenberg, R., Yarta, K., Staniloae, C., Williams, M. (2020) Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine. Clin. Immunol. 219:108544. PMID: 32707089; PMCID: PMC7374140.
187. Pillittere, J., Mian, S., Richardson, T.E., and Perl, A. (2020) Hydroxychloroquine-Induced Toxic Myopathy Causing Diaphragmatic Weakness and Lung Collapse Requiring Prolonged Mechanical Ventilation. J. Investig. Med. High Impact Case Rep. doi: 10.1177/2324709620950113; PMID: 32787461; PMCID: PMC7427040
188. Kato, H. and Perl, A. (2021) Double-Edged Sword: Interleukin-2 Promotes T regulatory Cell Differentiation but Expands Interleukin-13- and Interferon-γ-producing CD8+ T cells via STAT6-GATA-3 Axis in Systemic Lupus Erythematosus. Front. Immunol. PMID: 33763079;
189. Klionsky, D.H…Perl, A… (2021) Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition). Autophagy. 12: 1-382. PMID: 33634751; PMCID: PMC7996087
190. Piranavan, P. and Perl, A. (2021) Improvement of renal and non-renal SLE outcome measures on sirolimus therapy – a 21-year follow-up study of 73 patients. Clin. Immunol. 229:108781. PMID: 34144197;
191. Geier, C. and Perl A. (2021). Therapeutic mTOR blockade in systemic autoimmunity: implications for antiviral immunity and extension of lifespan. Autoimmun. Rev. 20:102984. PMID: 34718162; PMCID: PMC8550885
192. Nasr, S, Khalil, S, Poiesz, B, Banki, K, Perl, A. (2021) Pfizer-BioNTech COVID‑19 RNA vaccination induces phosphatidylserine autoantibodies, cryoglobulinemia, and digital necrosis in a patient with pre-existing autoimmunity. Clin. Immunol. Commun. 1:1-3.
193. Patel, A. and Perl, A. (2022). Redox control of integrin-mediated hepatic inflammation in systemic autoimmunity. Antioxid. Redox Signal. 36: 367-388. PMID: 34036799
194. Levack, R.C., Newell, K.L., Cabrera-Martinez, B., Cox, J., Perl, A., Bastacky, S.I. and Winslow, G.M. (2022) Adenosine Receptor 2a Agonists Target Mouse CD11c+Tbet+ B cells in Infection and Autoimmunity. Nat. Commun. 13:452. PMID: 35064115
195. Zhaomin, M, Tan, Y, Tao, J, Li, L, Wang, Hui, Yu, F., Perl, A. and Zhao, M. (2022). Renal mTORC1 Activation is Associated with Disease Activity and Prognosis in Lupus Nephritis. Rheumatology. 61:3830-3840. PMID: 35040950
196. El-Dokla, A., Bonilla, E. and Perl, A. (2022) Recurrent brachial plexopathy as initial presentation of systemic lupus erythematosus: a case report and review of the literature. Lupus, 31:500-504. PMID: 35259024
197. Caza, T., Wijewardena, C. Al-Rabadi, L. and Perl, A. (2022). Cell Type-Specific Mechanistic Target of Rapamycin-Dependent Distortion of Autophagy Pathways in Lupus Nephritis. Transl. Res. 245: 55-81. PMID: 35288362
198. Anuforo, A, Sandhu, M., Yu, J. and Perl, A. (2022) Appraising SARS-CoV-2 infections after full mRNA COVID-19 vaccination in patients with systemic lupus erythematosus (SLE). Clin. Immunol. Commun. 2:54-56.
199. Brown, J., Abboud, G., Ma, L., Choi, S-C., Kanda, N., Zeumer-Spataro, L., Lee, J., Peng, W., Cagmat, J., Faludi, T., Mohamadzadeh, M., Garrett, T., Mandik-Nayak, L., Chervonsky, A., Perl, A., and Morel, L. (2022). Microbiota-mediated skewing of tryptophan catabolism modulates CD4+ T cells in lupus-prone mice. iScience, 25:104241. PMID: 35494242; PMCID: PMC9051618
200. Perl, A., Agmon-Levin, N., Crispín, J.C. and Jorgensen, T.N. (2022) New Biomarkers for the Diagnosis and Treatment of Systemic Lupus Erythematosus: Connecting the dots between multi-omics and systems biology. Editorial. Front. Immunol. 13:1009038. PMID: 36311710; PMCID: PMC9599399
201. Nasr, S. and Perl, A. (2022) Principles behind SLE treatment with N-acetylcysteine. Immunometabolism, 4:e00010. PMID: 36312742; PMCID: PMC9605192
202. Oaks, Z, Patel, A, Huang, N, Choudhary, G, Winans, T, Faludi, T, Krakko, D, Duarte, M, Lewis, J, Beckford, M, Blair, S, Kelly, R, Landas, SK, Middleton, FA, Asara, JM, Chung, SK, Fernandez, DR, Banki, K, and Perl, A. (2023) Cytosolic aldose metabolism contributes to progression from cirrhosis to hepatocarcinogenesis. Nat. Metab. 5:41-60. PMID: 36658399;
203. Grossman, C. E. and Perl, A. (2023) Involvement of the pentose phosphate pathway in adipocyte differentiation: transaldolase expression is selectively up-regulated during phase of lipogenesis. Submitted.

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