The greatest contribution to medical science is the transformation from studying symptoms to studying their causes-the unrelenting legacy of Robert Koch and Louis Pasteur-and a causality perspective to approach a definition of SLE.

The basic initiative related to this study is derived from the fact that systemic lupus erythematosus (SLE) is a unique and fertile system science subject. We are, however, still far from understanding its nature. It may be fair to indicate that we are spending more time and resources on studying the complexity of classified SLE than studying the validity of classification criteria. This study represents a theoretical analysis of current instinctual SLE classification criteria based on "the causality principle." The discussion has its basis on the radical scientific traditions introduced by Robert Koch and Louis Pasteur. They announced significant changes in our thinking of disease etiology through the implementation of the modern version of "the causality principle." They influenced all aspects of today's medical concepts and research: the transformation of medical science from studies of symptoms to study their causes, relevant for monosymptomatic diseases as for syndromes. Their studies focused on bacteria as causes of infectious diseases and on how the immune system adapts to control and prevent contagious spreading. This is the most significant paradigm shift in the modern history of medicine and resulted in radical changes in our view of the immune system. They described acquired post-infection immunity and active immunization by antigen-specific vaccines. The paradigm "transformation" has a great theoretical impact also on current studies of autoimmune diseases like SLE: symptoms and their cause(s). In this study, the evolution of SLE classification and diagnostic criteria is discussed from "the causality principle" perspective, and if contemporary SLE classification criteria are as useful as believed today for SLE research. This skepticism is based on the fact that classification criteria are not selected based on cogent causal strategies. The SLE classification criteria do not harmonize with Koch's and Pasteur's causality principle paradigms and not with Witebsky's Koch-derived postulates for autoimmune and infectious diseases. It is not established whether the classification criteria can separate SLE as a "one disease entity" from "SLE-like non-SLE disorders"-the latter in terms of SLE imitations. This is discussed here in terms of weight, rank, and impact of the classification criteria: Do they all originate from "one basic causal etiology"? Probably not.

The influence and therapeutic effect of microbiota in systemic lupus erythematosus.

Systemic erythematosus lupus (SLE) is an autoimmune disease involving multiple organs that poses a serious risk to the health and life of patients. A growing number of studies have shown that commensals from different parts of the body and exogenous pathogens are involved in SLE progression, causing barrier disruption and immune dysregulation through multiple mechanisms. However, they sometimes alleviate the symptoms of SLE. Many factors, such as genetic susceptibility, metabolism, impaired barriers, food, and sex hormones, are involved in SLE, and the microbiota drives the development of SLE either by depending on or interacting with these factors. Among these, the crosstalk between genetic susceptibility, metabolism, and microbiota is a hot topic of research and is expected to lay the groundwork for the amelioration of the mechanism, diagnosis, and treatment of SLE. Furthermore, the microbiota has great potential for the treatment of SLE. Ideally, personalised therapeutic approaches should be developed in combination with more specific diagnostic methods. Herein, we provide a comprehensive overview of the role and mechanism of microbiota in lupus of the intestine, oral cavity, skin, and kidney, as well as the therapeutic potential of the microbiota.

Fascitis necrotizante asociada a esteatohepatitis en el curso del lupus eritematoso sistémico / Necrotizing Fasciitis Associated with Steatohepatitis in The Course of Systemic Lupus Erythematosus

Introducción: La fascitis necrotizante es un cuadro muy grave causado por una infección bacteriana de la piel y de tejidos blandos subcutáneos, cuya evolución es hacia la destrucción y necrosis de los tejidos en un corto espacio de tiempo; el lupus eritematoso sistémico es una enfermedad autoinmune de causa desconocida que quienes la padecen tienen una mayor probabilidad de contraer infecciones debido al mal funcionamiento del sistema inmunológico y/o los efectos secundarios causados por los medicamentos. Objetivo: Observar la importancia de un tratamiento rápido y eficaz de la fascitis necrotizante en un paciente con lupus eritematoso sistémico y esteatohepatitis no alcohólica. Presentación de caso: Se presentó el caso clínico de un paciente de 30 años con diagnóstico de lupus eritematoso sistémico que desarrolló de forma concomitante de fascitis necrotizante y esteatohepatitis no alcohólica. A pesar de un tratamiento adecuado, el paciente fue agresivo. Tuvo una estadía hospitalaria de 83 días, con una evolución desfavorable que conllevó a la muerte(AU)

Introduction: Necrotizing fasciitis is a very serious condition caused by a bacterial infection of the skin and subcutaneous soft tissues, whose evolution is towards the destruction and necrosis of the tissues in a short space of time; Systemic lupus erythematosus is an autoimmune disease of unknown cause that sufferers are more likely to contract infections due to poor immune system function and/or side effects caused by medications. Objective: To observe the importance of rapid and effective treatment of necrotizing fasciitis in a patient with systemic lupus erythematosus and non-alcoholic steatohepatitis. Case report: We report the clinical case of a 30-year-old patient diagnosed with systemic lupus erythematosus who concomitantly developed necrotizing fasciitis and nonalcoholic steatohepatitis. Despite adequate treatment, the patient was aggressive. The patient had a hospital stay of 83 days, with an unfavorable evolution that led to his death(AU)

Efficacy and safety of acupuncture therapy combined with conventional pharmacotherapy in the treatment of systemic lupus erythematosus: A systematic review and meta-analysis.

BACKGROUND: Currently, the mainstream treatments for systemic lupus erythematosus (SLE) are based on glucocorticoids and immunosuppressants, which are known to have considerable adverse effects. This meta-analysis is aimed at confirming the efficacy and safety of acupuncture therapy in combination with traditional medications in the treatment of SLE. METHODS: Multiple databases were searched for randomized controlled trials using acupuncture therapy in combination with conventional pharmacotherapy for the treatment of SLE, from the establishment of the database to March 2023. Study selection, data collection, as well as quality assessment were conducted by 2 reviewers independently. RevMan 5.4 and Stata 17 software were used for Meta-analysis. RESULTS: Seven eligible studies involving 514 patients with SLE were included. Meta-analysis demonstrated that in SLE patients, extra treatment with acupuncture was superior to drug therapy alone in improving the overall response rate (RR = 1.20, 95% confidence intervals [1.11, 1.29], P < .00001, heterogeneity P = .69, I2 = 0%) and regulating immunological indicators (C3, C4, IgG, T lymphocyte subpopulation, IL-6, ds-DNA, ESR) while reducing TCM symptom scores, the SLE Disease Activity Index (SLEDAI) and the incidence of adverse events on treatment (P ≤ 0.05). Additionally, it was able to reduce BUN, Scr and 24 hours urine protein, suggesting that acupuncture treatment had a protective effect on the kidneys. CONCLUSIONS: Acupuncture therapy combined with conventional pharmacotherapy is an efficient and safe way in the treatment of SLE. However, the conclusions drawn from this meta-analysis have some limitations due to the small number and uneven quality of the included studies, leading to heterogeneity and bias. Thus more relevant high-quality randomized controlled trials are needed for further evaluation in the future.

The Role of Neutrophil Extracellular Traps (NETs) in the Pathogenesis of Systemic Lupus Erythematosus and Antiphospholipid Syndrome.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease of unknown aetiology [...].

The Disease with a Thousand Faces and the Human Microbiome-A Physiopathogenic Intercorrelation in Pediatric Practice.

Numerous interrelationships are known in the literature that have the final effect of unmasking or influencing various pathologies. Among these, the present article aims to discuss the connection between systemic lupus erythematosus (SLE) and the human microbiome. The main purpose of this work is to popularize information about the impact of dysbiosis on the pathogenesis and evolutionary course of pediatric patients with SLE. Added to this is the interest in knowledge and awareness of adjunctive therapeutic means that has the ultimate goal of increasing the quality of life. The means by which this can be achieved can be briefly divided into prophylactic or curative, depending on the phase of the condition in which the patient is. We thus reiterate the importance of the clinician acquiring an overview of SLE and the human microbiome, doubled by in-depth knowledge of the physio-pathogenic interactions between the two (in part achieved through the much-studied gut-target organ axes-brain, heart, lung, skin), with the target objective being that of obtaining individualized, multimodal and efficient management for each individual patient.

Environmental risk factors of systemic lupus erythematosus: a case-control study.

Systemic lupus erythematosus (SLE) is a complicated chronic autoimmune disorder. Several genetic and environmental factors were suggested to be implicated in its pathogenesis. The main objective of this study was to examine how exposure to selected environmental factors was associated with SLE risk to support the development of disease preventive strategies. A case-control study was conducted at the Rheumatology outpatient clinic of Alexandria Main University Hospital, in Alexandria, Egypt. The study sample consisted of 29 female SLE patients, and 27 healthy female controls, who matched the cases on age and parity. Data were collected by a structured interviewing questionnaire. Blood levels of lead, cadmium, and zinc of all participants were assessed by flame atomic absorption spectrometry. The multivariate stepwise logistic regression model revealed that five factors showed significant association with SLE, namely living near agricultural areas, passive smoking, blood lead levels ≥ 0.075 mg/L, and exposure to sunlight (odds ratio (OR) 58.556, 95% confidence interval (CI) 1.897-1807.759, OR 24.116, 95% CI 1.763-329.799, OR 18.981, 95% CI 1.228-293.364, OR 9.549, 95% CI 1.299-70.224, respectively). Whereas walking or doing exercise were significantly protective factors (P = 0.006). The findings of this study add to the evidence that SLE can be environmentally induced. Preventive measures should be taken to address the environmental risk factors of SLE.

Climatério e lúpus eritematoso sistêmico / Climacteric and systemic lupus erythematosus

O lúpus eritematoso sistêmico é uma doença crônica, complexa e multifatorial que apresenta manifestações em vários órgãos. O seu acometimento ocorre 10 vezes mais no sexo feminino do que no masculino. É uma doença com uma clínica variada e com graus variados de gravidade, causando fadiga, manifestações cutâneas, como rash malar, fotossensibilidade, queda de cabelo e manifestações musculoesqueléticas, como artralgia, mialgia e atrite. Podem ocorrer flares (crises), que se caracterizam por aumento mensurável na atividade da doença. No climatério, no período da pré-menopausa, o lúpus eritematoso sistêmico ocorre com mais frequência, podendo ocorrer também na pós-menopausa. Algumas doenças são mais frequentes na fase do climatério, e a presença do lúpus pode influenciar na sua evolução, como a doença cardiovascular, osteoporose e tromboembolismo venoso. A terapia hormonal oral determina aumento do risco de tromboembolismo venoso no climatério, e na paciente com lúpus eritematoso sistêmico há aumento dos riscos de flares e de trombose. Em vista disso, a terapia hormonal é recomendada apenas para pacientes com lúpus eritematoso sistêmico estável ou inativo, sem história de síndrome antifosfolípides e com anticorpos antifosfolípides negativa, devendo-se dar preferência para a terapia estrogênica transdérmica, em menor dose e de uso contínuo. Na paciente com lúpus eritematoso sistêmico ativo ou com história de síndrome antifosfolípides ou com anticorpos antifosfolípides positiva, recomenda-se a terapia não hormonal, como os antidepressivos. (AU)

Systemic lupus erythematosus is a chronic, complex, multifactorial disease that manifests in several organs. Its involvement occurs 10 times more in females than in males. It is a disease with a varied clinic and varying degrees of severity, causing fatigue, skin manifestations such as malar rash, photosensitivity, hair loss and musculoskeletal manifestations such as arthralgia, myalgia and arthritis. Flare may occur, which are characterized by measurable increase in disease activity. In the climacteric, in the premenopausal period, systemic lupus erythematosus occurs more frequently, and may also occur in the postmenopausal period. Some diseases are more frequent in the Climacteric phase and the presence of lupus can influence its evolution, such as cardiovascular disease, osteoporosis and venous thromboembolism. Oral hormone therapy determines an increased risk of venous thromboembolism in the climacteric and in patients with systemic lupus erythematosus there is an increased risk of flares and thrombosis. In view of this, hormone therapy is only recommended for patients with stable or inactive systemic lupus erythematosus, without a history of antiphospholipid syndrome and with antiphospholipid antibodies, giving preference to transdermal estrogen therapy, at a lower dose and for continuous use. In patients with active systemic lupus erythematosus or with a history of antiphospholipid syndrome or positive antiphospholipid antibodies, non-hormonal therapy, such as antidepressants, is recommended. (AU)

Advances in the Pathogenesis and Treatment of Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) is a genetically predisposed, female-predominant disease, characterized by multiple organ damage, that in its most severe forms can be life-threatening. The pathogenesis of SLE is complex and involves cells of both innate and adaptive immunity. The distinguishing feature of SLE is the production of autoantibodies, with the formation of immune complexes that precipitate at the vascular level, causing organ damage. Although progress in understanding the pathogenesis of SLE has been slower than in other rheumatic diseases, new knowledge has recently led to the development of effective targeted therapies, that hold out hope for personalized therapy. However, the new drugs available to date are still an adjunct to conventional therapy, which is known to be toxic in the short and long term. The purpose of this review is to summarize recent advances in understanding the pathogenesis of the disease and discuss the results obtained from the use of new targeted drugs, with a look at future therapies that may be used in the absence of the current standard of care or may even cure this serious systemic autoimmune disease.

Multisite chronic pain and the risk of autoimmune diseases: A Mendelian randomization study.

Background: Accumulating evidence has demonstrated that an association between chronic pain and autoimmune diseases (AIDs). Nevertheless, it is unclear whether these associations refer to a causal relationship. We used a two-sample Mendelian randomization (MR) method to determine the causal relationship between chronic pain and AIDs. Methods: We assessed genome-wide association study (GWAS) summary statistics for chronic pain [multisite chronic pain (MCP) and chronic widespread pain (CWP)], and eight common AIDs, namely, amyotrophic lateral sclerosis (ALS), celiac disease (CeD), inflammatory bowel disease (IBD), multiple sclerosis (MS), rheumatoid arthritis (RA), systemic lupus Erythematosus (SLE), type 1 diabetes (T1D) and psoriasis. Summary statistics data were from publicly available and relatively large-scale GWAS meta-analyses to date. The two-sample MR analyses were first performed to identify the causal effect of chronic pain on AIDs. The two-step MR and multivariable MR were used to determine if mediators (BMI and smoking) causally mediated any connection and to estimate the proportion of the association mediated by these factors combined. Results: With the utilization of MR analysis, multisite chronic pain was associated with a higher risk of MS [odds ratio (OR) = 1.59, 95% confidence interval (CI) = 1.01-2.49, P = 0.044] and RA (OR = 1.72, 95% CI = 1.06-2.77, P = 0.028). However, multisite chronic pain had no significant effect on ALS (OR = 1.26, 95% CI = 0.92-1.71, P = 0.150), CeD (OR = 0.24, 95% CI = 0.02-3.64, P = 0.303), IBD (OR = 0.46, 95% CI = 0.09-2.27, P = 0.338), SLE (OR = 1.78, 95% CI = 0.82-3.88, P = 0.144), T1D (OR = 1.15, 95% CI = 0.65-2.02, P = 0.627) or Psoriasis (OR = 1.59, 95% CI = 0.22-11.26, P = 0.644). We also found positive causal effects of MCP on BMI and causal effects of BMI on MS and RA. Moreover, there were no causal connections between genetically predicted chronic widespread pain and the risk of most types of AIDs disease. Conclusion: Our MR analysis implied a causal relationship between MCP and MS/RA, and the effect of MCP on MS and RA may be partially mediated by BMI.

Interferons and systemic lupus erythematosus: Pathogenesis, clinical features, and treatments in interferon-driven disease.

Type I interferons (IFNs) have recently received a lot of attention with the elucidation of the pathogenesis of systemic lupus erythematosus (SLE). Type I IFNs are associated with many SLE symptoms and play a role in the pathogenesis of autoimmune diseases that may occur concurrently with SLE, such as Sjögren's syndrome, antiphospholipid syndrome, myositis, scleroderma, and interferonopathy. Type I IFNs could be the link between these diseases. However, direct measurement of type I IFN levels and the IFN gene signature is currently unavailable in clinical practice. This review discusses type I IFN signalling in SLE, investigates the role of type I IFN in the clinical manifestations and symptoms associated with SLE and other IFN-related diseases, and discusses the clinical tests that can be used to diagnose SLE and measure disease activity. In addition, the role of type I IFN-blocking therapies as potential treatments for SLE is discussed.

Association of Sleep Deprivation and the Risk of Developing Systemic Lupus Erythematosus Among Women.

OBJECTIVE: Sleep deprivation has been associated with risk of autoimmune diseases. Using the Nurses' Health Study (NHS) (1986-2016) and NHSII (1989-2017) cohorts, we aimed in the present study to investigate whether sleep deprivation was associated with risk of developing systemic lupus erythematosus (SLE). METHODS: Average sleep duration in a 24-hour period was reported in the NHS (1986-2014) and NHSII (1989-2009). Lifestyle, exposure, and medical information was collected on biennial questionnaires. Adjusted Cox regression analyses modeled associations between cumulative average sleep duration (categorical variables) and incident SLE. Interactions between sleep duration and shiftwork, bodily pain (using the Short Form 36 [SF-36] questionnaire), and depression were examined. RESULTS: We included 186,072 women with 187 incident SLE cases during 4,246,094 person-years of follow-up. Chronic low sleep duration (≤5 hours/night versus reference >7-8 hours) was associated with increased SLE risk (adjusted hazard ratio [HRadj ] 2.47 [95% confidence interval (95% CI) 1.29, 4.75]), which persisted after the analysis was lagged (4 years; HRadj 3.14 [95% CI 1.57, 6.29]) and adjusted for shiftwork, bodily pain, and depression (HRadj 2.13 [95% CI 1.11, 4.10]). We detected additive interactions between low sleep duration and high bodily pain (SF-36 score <75) with an attributable proportion (AP) of 64% (95% CI 40%, 87%) and an HR for SLE of 2.97 (95% CI 1.86, 4.75) for those with both risk factors compared to those with neither. Similarly, there was an interaction between low sleep duration and depression, with an AP of 68% (95% CI 49%, 88%) and an HR for SLE of 2.82 (95% CI 1.64, 4.85). CONCLUSION: Chronic low sleep duration was associated with higher SLE risk, with stronger effects among those with bodily pain and depression, highlighting the potential role of adequate sleep in disease prevention.

The impact of the gut microbiome on extra-intestinal autoimmune diseases.

The prevalence of autoimmune diseases (ADs) worldwide has rapidly increased over the past few decades. Thus, in addition to the classical risk factors for ADs, such as genetic polymorphisms, infections and smoking, environmental triggers have been considered. Recent sequencing-based approaches have revealed that patients with extra-intestinal ADs, such as multiple sclerosis, rheumatoid arthritis, type 1 diabetes and systemic lupus erythematosus, have distinct gut microbiota compositions compared to healthy controls. Faecal microbiota transplantation or inoculation with specific microbes in animal models of ADs support the hypothesis that alterations of gut microbiota influence autoimmune responses and disease outcome. Here, we describe the compositional and functional changes in the gut microbiota in patients with extra-intestinal AD and discuss how the gut microbiota affects immunity. Moreover, we examine how the gut microbiota might be modulated in patients with ADs as a potential preventive or therapeutic approach.

Association of Ultraviolet B Radiation and Risk of Systemic Lupus Erythematosus Among Women in the Nurses' Health Studies.

OBJECTIVE: Ultraviolet (UV) radiation exposure is associated with photosensitivity, rashes, and flares in systemic lupus erythematosus (SLE). However, it is not known whether UV exposure increases risk of developing SLE. We examined UV exposure and SLE risk in a large prospective cohort. METHODS: The Nurses' Health Study (NHS) enrolled 121,700 US female nurses in 1976; in 1989, 116,429 nurses were enrolled in NHS II. Biennial questionnaires collected lifestyle and medical data. Self-reported incident SLE by American College of Rheumatology classification criteria was confirmed by medical record review. Ambient UV exposure was estimated by linking geocoded residential addresses with a spatiotemporal UV exposure model. Cox models estimated hazard ratios (HRs) and 95% confidence intervals (95% CIs) across tertiles of time-varying cumulative average UV. We examined SLE risk overall and stratified by anti-Ro/La antibodies and by cutaneous manifestations from 1976 through 2014 (NHS)/2015 (NHS II), adjusting for confounders. RESULTS: With 6,054,665 person-years of exposure, we identified 297 incident SLE cases; the mean ± SD age at diagnosis was 49.8 ± 10.6 years. At diagnosis, 16.8% of women had +anti-Ro/La, and 80% had either +anti-Ro/La or ≥1 cutaneous manifestation. Compared with the lowest UV exposure tertile, risk of overall SLE was increased, but not significantly (HR 1.28 [95%CI 0.96-1.70]). Women in the highest tertile had increased risk of malar rash (HR 1.62 [95% CI 1.04-2.52]). CONCLUSION: Cumulative UV exposure was not associated with SLE risk. Higher UV exposure, however, was associated with increased risk of malar rash at presentation. UV exposure may trigger SLE onset with malar rash among susceptible women.

Systemic Lupus Erythematosus Risk: The Role of Environmental Factors.

Systemic lupus erythematosus (SLE) is a complex, chronic autoimmune disease. The etiology of SLE is multifactorial and includes potential environmental triggers, which may occur sequentially (the "multi-hit" hypothesis). This review focuses on SLE risk potentially associated with environmental factors including infections, the microbiome, diet, respirable exposures (eg, crystalline silica, smoking, air pollution), organic pollutants, heavy metals, and ultraviolet radiation.

Role of air pollution in systemic lupus erythematosus. / 空气污染在系统性红斑狼疮发生发展中的作用.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease that can affect almost every organ in the human body. The etiology and pathogenesis are unclear. Recent studies have shown that pathogenesis and development of SLE result from the interaction between various internal and external factors. Current studies suggest that air pollution may increase the risk of SLE through multiple mechanisms such as inducing immune disorders, causing epigenetic changes, and inducing oxidative stress. Air pollution has a certain relationship with pulmonary interstitial lesions, lupus nephritis, decreased reproductive function and other system damages in SLE patients, and it is related to the occurrence and clinical outcomes of SLE. Air pollution has a potential role in the occurrence and development of SLE, providing a brand-new view on the early prevention and control of SLE.

Will fecal microbiota transplantation eventually be an effective therapeutic strategy for systemic lupus erythematosus?

Gut microbiota dysbiosis serves as a potential trigger that may contribute to metabolic and immune dysregulation that underlies the development of autoimmune diseases. Fecal microbiota transplantation (FMT) is restoration of disturbed microbiota by transplanting foreign gut microbiota from healthy individuals into the gastrointestinal tract of diseased individuals. In this issue of the Journal of Autoimmunity, Huang et al. conducted a 12-week, single-arm pilot clinical trial of oral FMT capsules in patients with active SLE. No serious adverse events (AEs) or deaths were observed and the rate of the primary endpoint (SLE Responder Index-4) was 42.12%. Alternations in bacteria, metabolites and immune parameters were linked to FMT treatment and clinical response in SLE patients. This is the first FMT trial in SLE patients and provides supportive evidence that FMT appears to be a safe, feasible and potentially effective treatment modality in SLE. We await future investigations conducting larger, randomized FMT clinical trials with a longer follow-up to confirm the long-term safety, effectiveness, and potential benefits of FMT-based intervention in SLE and to further demonstrate the underlying microbiological mechanisms.

Systemic lupus erythematosus following human papillomavirus vaccination: A case-based review.

Systemic lupus erythematosus (SLE) is a heterogeneous systemic autoimmune diseases (AIDs) with many pathogenic factors, ranging from genetic to epigenetic to environmental. The human papillomavirus (HPV), a viral infectious agent, is a common contributor to the onset and exacerbation of SLE. HPV infections are more prevalent among SLE patients than healthy individuals, bringing about a substantial need for treatment. While HPV recombinant gene vaccines are accepted as a universal method for infection prevention, they pose a risk for adverse events such as fever, joint pain, and rashes. In rare cases, they might even trigger AIDs such as SLE, especially in patients with a personal or family history of such diseases. In this article, we provide a report of a case of SLE onset following HPV vaccination and a review of 11 similar cases. An analysis of 12 patients revealed that 7 cases of SLE developed between 3 weeks and 2 months post-vaccination. Symptoms of SLE generally manifest as fatigue, fever, joint pain, and myalgia. Two patients had lupus nephritis, 2 showed central nervous system involvement, including abnormal behavior and epileptic seizures, and 1 had intestinal pseudo-obstruction. All patients showed rapid remission with glucocorticoid and immunosuppressive therapy and remained stable during several months of follow-up.

Abnormalities of T cells in systemic lupus erythematosus: new insights in pathogenesis and therapeutic strategies.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by loss of immune tolerance and sustained production of autoantibodies. Multiple and profound T cell abnormalities in SLE are intertwined with disease expression. Both numerical and functional disturbances have been reported in main CD4+ T helper cell subsets including Th1, Th2, Th17, regulatory, and follicular helper cells. SLE CD4+ T cells are known to provide help to B cells, produce excessive IL-17 but insufficient IL-2, and infiltrate tissues. In the absence of sufficient amounts of IL-2, regulatory T cells, do not function properly to constrain inflammation. A complicated series of early signaling defects and aberrant activation of kinases and phosphatases result in complex cell phenotypes by altering the metabolic profile and the epigenetic landscape. All main metabolic pathways including glycolysis, glutaminolysis and oxidative phosphorylation are altered in T cells from lupus prone mice and patients with SLE. SLE CD8+ cytotoxic T cells display reduced cytolytic activity which accounts for higher rates of infection and the sustenance of autoimmunity. Further, CD8+ T cells in the context of rheumatic diseases lose the expression of CD8, acquire IL-17+CD4-CD8- double negative T (DNT) cell phenotype and infiltrate tissues. Herein we present an update on these T cell abnormalities along with underlying mechanisms and discuss how these advances can be exploited therapeutically. Novel strategies to correct these aberrations in T cells show promise for SLE treatment.