Autoimmunity Reviews[JOURNAL]
Sun
200 papers
Advancing research on regulatory autoantibodies targeting GPCRs: Insights from the 5th international symposium.
Cabral-Marques O, Schimke LF, Moll G … +57 more , Filgueiras IS, Nóbile AL, Adri AS, do Vale FYN, Usuda JN, Corrêa YLG, Albuquerque D, Nava RG, Santos RS, Dias HD, Silva HF, Marconi PB, Catar R, Adu-Gyamfi M, Wang P, Khan TA, Hackel AM, Leheis A, Stähle A, Müller A, Schmidt C, Radunovic C, Adjailia EB, Grasshoff H, Humrich JY, Menz J, Fourlakis K, Winziers M, Jäpel M, Wegner MV, Lamprecht P, Nieberding R, Akbarzadeh R, Arnold S, Jendrek S, Klapa S, Augustin S, Biedermann S, Schinke S, Scheerer P, Endres M, Schulze-Forster K, Paul F, Yu X, Sotzny F, Sakmar TP, Banasik M, Haghikia A, Hoffmann MH, Veprintsev D, Witte T, Dalmolin RJS, Ochs HD, Heidecke H, Scheibenbogen C, Shoenfeld Y, Riemekasten G
Autoimmun Rev · 2025 Aug · PMID 40543860 · Publisher ↗
The 5th International Symposium on Regulatory Autoantibodies Targeting GPCR (RAB-GPCRs) advanced the understanding of the significant role played by autoantibodies targeting G-protein-coupled receptors (GPCRs) in various...
The 5th International Symposium on Regulatory Autoantibodies Targeting GPCR (RAB-GPCRs) advanced the understanding of the significant role played by autoantibodies targeting G-protein-coupled receptors (GPCRs) in various human diseases. Once considered passive markers, RAB-GPCRs are now recognized as active modulators of cellular signaling, immune regulation, and inflammation. The symposium highlighted their involvement in multiple prominent pathologies, including autoimmune diseases, cardio- and cerebrovascular diseases, and neuroimmunologic disorders such as myalgic encephalomyelitis/chronic fatigue syndrome and post-COVID-19 syndrome (ME/CFS/PCS), as well as solid organ and hematopoietic stem cell transplantation (SOT/HSCT). Experts from rheumatology, immunology, and neurology presented interdisciplinary discussions on the potential of RAB-GPCRs as biomarkers and therapeutic targets. Advances in screening methods, biomarker identification, and therapeutic strategies were shared, emphasizing their diagnostic potential and application in novel therapeutic interventions. This report summarizes key insights from the symposium, particularly focusing on the modulatory properties of RAB-GPCRs and their relevance in both immune-mediated diseases and other pathologies (e.g., vascular, degenerative) that are traditionally not considered primarily immune-mediated. Ongoing research is expected to further establish these autoantibodies as crucial components in disease modulation and systems biology contexts, offering new opportunities for precision medicine and improved clinical outcomes in immune-related disorders.
Systematic evaluation of the associations between schizophrenia and autoimmune diseases: An umbrella review.
Sun Z, Han B, Ding Q … +8 more , Feng Y, Jia T, Ouyang Y, Guo X, Liang J, Huang Q, Kou C, Bai W
Autoimmun Rev · 2025 Aug · PMID 40532773 · Publisher ↗
OBJECTIVE: This study aims to assess research trends in the association between schizophrenia and autoimmune diseases, systematically review their relationship, and evaluate the credibility of existing evidence. METHODS:...
OBJECTIVE: This study aims to assess research trends in the association between schizophrenia and autoimmune diseases, systematically review their relationship, and evaluate the credibility of existing evidence. METHODS: Bibliometric analysis was conducted using the bibliometrix package in R, along with VOSviewer and CiteSpace. Relevant systematic reviews and meta-analyses were retrieved from six databases: PubMed, Web of Science, Embase, CINAHL, PsycINFO, and the Cochrane Library. Summary risk estimates were recalculated using the DerSimonian and Laird method under a random-effects model, and the credibility of the evidence was assessed. RESULTS: The bibliometric analysis found that "meta-analysis" has become a frequently used keyword and may be a focal point for future research. The umbrella review included 17 articles, containing 24 report data points from 12 quantitative reviews. Results indicated that 9 reports assessed the relationship between schizophrenia and autoimmune diseases. Schizophrenia was significantly associated with autoimmune neurological disorders (RR = 1.42; 95 % CI = 1.18-1.72), providing suggestive evidence. Seven reports evaluated the impact of schizophrenia on autoimmune diseases, showing highly suggestive evidence that schizophrenia patients had a pooled relative risk of 2.22 (95 % CI = 1.95-2.52) for psoriasis. Eight reports assessed the impact of autoimmune diseases on schizophrenia, with bullous pemphigoid patients showing significantly higher schizophrenia prevalence (OR = 2.63; 95 % CI = 2.03-3.39). CONCLUSIONS: This study synthesizes evidence of varying levels, highlighting the association between schizophrenia and autoimmune diseases. It offers new insights for future exploration, fosters interdisciplinary collaboration, and provides valuable implications for public health policy development.
Clinical features, pathogenesis, and treatment of inflammatory bowel disease-associated spondyloarthritis.
Akiyama M, Alshehri W, Suzuki K … +3 more , Shimanuki K, Saito K, Kaneko Y
Autoimmun Rev · 2025 Aug · PMID 40527403 · Publisher ↗
Inflammatory bowel disease-associated spondyloarthritis (IBD-SpA) is a unique subtype of SpA that affects approximately 10-20 % of patients with IBD. It encompasses both peripheral arthritis and axial involvement, with e...
Inflammatory bowel disease-associated spondyloarthritis (IBD-SpA) is a unique subtype of SpA that affects approximately 10-20 % of patients with IBD. It encompasses both peripheral arthritis and axial involvement, with enthesitis being increasingly recognized. Despite its clinical significance, there are currently no established screening tools, classification criteria, or standardized treatment guidelines specific to IBD-SpA. Management is typically guided by recommendations for IBD and SpA, requiring close collaboration between gastroenterologists and rheumatologists. Emerging evidence suggests that subclinical gut inflammation and IL-23-IL-17-TNFα signaling pathway play central roles in the pathogenesis of IBD-SpA. Among the available therapeutic options, TNF inhibitors and JAK inhibitors have demonstrated efficacy in both IBD and SpA, whereas IL-17 inhibitors may exacerbate intestinal inflammation. Additionally, vedolizumab, an α4β7 integrin inhibitor, while effective for IBD, has been implicated in triggering de novo SpA. These complexities highlight the need for a tailored treatment approach that balances efficacy for both gut and joint inflammation. This review provides an updated overview of the clinical features, diagnosis, pathogenesis, and treatment strategies for IBD-SpA, emphasizing recent advancements and future directions in the field.
The role of B cells in Sjögren's syndrome and their impact on the nervous system.
Su C, Wang W, Cheng F … +2 more , Zhao F, Zheng SG
Autoimmun Rev · 2025 Jul · PMID 40494441 · Publisher ↗
Primary Sjögren's syndrome is an autoimmune disease characterized by the dryness of exocrine glands. Recent studies emphasizes the significant role of B cells in its pathogenesis. This review provides an overview of the...
Primary Sjögren's syndrome is an autoimmune disease characterized by the dryness of exocrine glands. Recent studies emphasizes the significant role of B cells in its pathogenesis. This review provides an overview of the functions of B cells in Sjögren's syndrome and their impact on the nervous system. Current studies on the association between B cell-mediated immune responses and neurological symptoms are reviewed, aiming to offer new insights for diagnosing and treating. Understanding these connections is crucial for addressing the complex interplay between the immune system and neurological manifestations in affected individuals. A critical gap remains in determining whether B cell dysregulation initiates neuropathology or amplifies pre-existing neural inflammation, highlighting the need for mechanistic studies to guide targeted therapies.
Autoreactive B cells in autoimmune diseases: Mechanisms, functions and clinical implications.
Collet A, Guerrier T, Sanges S … +4 more , Chépy A, Sobanski V, Launay D, Dubucquoi S
Autoimmun Rev · 2025 Jul · PMID 40494440 · Publisher ↗
Autoreactive B cells play a key role in the pathophysiology of autoimmune diseases (AIDs). Still, due to their low frequency in the circulating blood, they are less well characterized than the global B cell pool. This re...
Autoreactive B cells play a key role in the pathophysiology of autoimmune diseases (AIDs). Still, due to their low frequency in the circulating blood, they are less well characterized than the global B cell pool. This review aims at describing the tools that allow the study of autoreactive B cells, deciphering their features and functions, and discussing the therapeutic implications that arise from these findings. The capacity to detect and analyze autoreactive B cells has been significantly improved by diverse techniques such as ELISpot and flow cytometry, shedding light on their roles in immune dysregulation. It reveals the multifaceted features of autoreactive B cells in terms of phenotypic and functional characteristics, that vary between different AIDs, and from one autoantigen to another. This heterogeneity may be influenced by factors such as the nature of the targeted autoantigen, or the costimulatory signals involved. These observations highlight that autoreactive B cells contribute not only to autoantibody production, but also to the perpetuation of autoimmunity through additional mechanisms, including antigen presentation and cytokine secretion. Recent therapeutic approaches have been developed to target autoreactive B cells, allowing an antigen-specific depletion of B cells, without causing widespread immunosuppression. Challenges remain, such as understanding the precise mechanisms by which the B cell tolerance breakdown occur, and the pathways by which autoreactive B cells activate (i.e. germinal centre or extrafollicular pathway). Ongoing research into the mechanisms regulating autoreactive B cells will be crucial for designing more targeted and effective therapies, leading to better outcomes for AID patients.
Clostridioides difficile-related reactive arthritis: A scoping review of the literature.
Deligeorgakis D, Makri ES, Tsafis K … +5 more , Skouvaklidou E, Katsigianni I, Adamichou C, Kougkas N, Dimitroulas T
Autoimmun Rev · 2025 Jul · PMID 40484294 · Publisher ↗
Reactive arthritis (ReA) is an inflammatory arthritis triggered by preceding infection. While various bacterial pathogens are well-established as causative agents, the role of Clostridioides difficile remains less elucid...
Reactive arthritis (ReA) is an inflammatory arthritis triggered by preceding infection. While various bacterial pathogens are well-established as causative agents, the role of Clostridioides difficile remains less elucidated. Α scoping review was conducted to evaluate the existing literature on CDI-induced ReA to determine clinical features, management, and disease trajectory. Sixty-one CDI-related ReA cases were identified (61 % male, mean age 38.8 years). HLA-B27 positivity was 64 % (30/47 tested). Prior antibiotic use was reported in 89 % of cases, with arthritis onset 8.5 days post-CDI. Oligoarthritis predominated (41 %), involving a median of 3 joints (knee 67 %, ankle 44 %, hand 26 %). Extra-articular manifestations were present in 20 %. Only 10 % required treatment escalation to disease-modifying anti-rheumatic drugs (DMARDs). Remission was achieved in 87 % within 21 days, with 9 % relapse rate. HLA-B27 positive patients had fewer affected joints (2 vs 5, p = 0.03) and older age at onset (43.1 vs 29.1, p = 0.02). Pediatric patients were more likely to experience hip arthritis than adults (54 % vs 10 %, p = 0.003). This study confirms CDI as a cause of ReA, highlighting its typically benign course with high remission rates. Further research is warranted, particularly regarding refractory cases.
Corrigendum to "Safety of biologics in patients with autoimmune rheumatic diseases during pregnancy: Systematic review and meta-analysis" [Autoimmunity Reviews, Volume 24 (2025), Issue 8, /103827].
Li S, Liu H, Zeng S … +4 more , Xie J, Li Z, Yang Y, Chuan J
Autoimmun Rev · 2025 Jul · PMID 40482429 · Publisher ↗
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Genetic and immune dysregulation in vitiligo: Insights into autoimmune mechanisms and disease pathogenesis.
Upadhya S, Andrade MJ, Shukla V … +2 more , Rao R, Satyamoorthy K
Autoimmun Rev · 2025 Jul · PMID 40466982 · Publisher ↗
Vitiligo is a hypopigmentary skin disease condition affecting local melanocytes leading to the white patched/macules of depigmented skin due to their progressive loss of melanocytes in the epidermis. Vitiligo pathogenesi...
Vitiligo is a hypopigmentary skin disease condition affecting local melanocytes leading to the white patched/macules of depigmented skin due to their progressive loss of melanocytes in the epidermis. Vitiligo pathogenesis involves complex interaction of several trigger factors including genetic predispositions, environmental stimuli, oxidative stress, immunological dysregulation, and impaired melanocyte function. Genetic studies have provided insight into the essential aspects related to immunological modulation, melanocyte biology and the oxidative stress response, aiding in understanding the possible mechanisms underlying vitiligo susceptibility. Epigenetic modifications further contribute to the regulatory landscape controlling the pathophysiology of this disease. While genetic studies identified key susceptibility loci, it is the functional studies that have driven the development of novel targeted therapies. Although vitiligo exhibits complex heterogenous clinical manifestations and multiple contributing factors, significant advancements have been achieved in understanding the underlying mechanism of the disease. Particularly, cytotoxic T-cell activity and interferon-gamma (IFN-ϒ) mediated immune response have been studied extensively in disease pathogenesis. This has led to the development of novel targeted therapies including cytokine targeted therapies, Janus-activated kinase (JAK) signaling inhibitors, and Wnt signaling agonists which have shown potential clinical success.
Advances in precision medicine in imaging and therapeutic strategies for psoriatic disease.
Witte T, Minopoulou I, Drzeniek NM … +13 more , Torgutalp M, Sabat R, Casteleyn V, Albach F, Fagni F, Schett G, Zabotti A, Krönke G, McGonagle D, Köhm M, Behrens F, Kleyer A, Simon D
Autoimmun Rev · 2025 Jul · PMID 40456394 · Publisher ↗
Psoriatic disease, encompassing psoriasis (PsO) and psoriatic arthritis (PsA), affects approximately 2 % of the global population. In the majority of cases, skin alterations occur first, followed by musculoskeletal disor...
Psoriatic disease, encompassing psoriasis (PsO) and psoriatic arthritis (PsA), affects approximately 2 % of the global population. In the majority of cases, skin alterations occur first, followed by musculoskeletal disorders. The transition from cutaneous to synovio-entheseal disease reflects a gradual immune-driven progression from localized to systemic manifestations in most cases. Subclinical or non-specific symptoms often precede demonstrable synovitis or enthesitis, which further delays diagnosis and increases the risk of irreversible structural damage. Despite the critical importance of early detection, established risk factors for PsA are largely nonspecific, presenting challenges for precision medicine. Key amongst these is the presence of arthralgia, which usually precedes PsA development but is also common in degenerative and biomechanical problems. Recent advancements, encompassing cutting-edge imaging modalities, hold the potential to facilitate earlier and more precise detection of PsA, while groundbreaking therapeutic innovations are redefining treatment paradigms and may further integrate advanced imaging into personalized therapeutic strategies. This review explores the molecular and clinical complexity of psoriatic disease, highlights the latest developments in imaging and treatment, and considers their potential to revolutionize patient outcomes. Novel strategies promise advances in precision medicine and may pave the way for customized interventions that not only enhance the diagnosis and prognosis of psoriatic disease but also refine therapeutic decision-making. Innovative imaging techniques are essential to distinguishing psoriatic disease-related pain from alternative causes such as osteoarthritis, thereby guiding treatment continuation and optimization.
Dual B-cell targeting in systemic lupus erythematosus: The role of combined and sequential therapy with rituximab and belimumab.
Frade-Sosa B, Sarmiento-Monroy JC, Bruce IN … +2 more , Arnaud L, Gómez-Puerta JA
Autoimmun Rev · 2025 Jul · PMID 40414587 · Publisher ↗
Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by immune dysregulation and autoantibody production. Despite advances in treatment, achieving sustained disease control remains challenging...
Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by immune dysregulation and autoantibody production. Despite advances in treatment, achieving sustained disease control remains challenging. Rituximab (RTX) and belimumab (BELI) are two B-cell-targeting biologics with complementary mechanisms of action, leading to increasing interest in their combination as a therapeutic strategy for refractory SLE. RTX depletes CD20+ B cells, whereas BELI inhibits B-lymphocyte stimulator (BLyS), reducing the survival of autoreactive B cells. Sequential therapy with these agents may mitigate B-cell repopulation and improve disease control. Recent studies, including SynBioSe and BEAT-LUPUS, suggest that RTX-BELI therapy can reduce autoantibody levels, neutrophil extracellular trap formation, and disease activity, with many patients achieving a lupus low disease activity state (LLDAS). However, the BLISS-BELIEVE and CALIBRATE trials did not demonstrate superiority over monotherapy, highlighting the need to refine patient selection. Combination therapy may be particularly beneficial in lupus nephritis, where BELI delays autoreactive B-cell reconstitution following RTX, potentially prolonging remission. While RTX-BELI therapy is generally well-tolerated, some studies report increased infections, necessitating careful patient monitoring. Lessons from other immune-mediated diseases, including inflammatory bowel disease and rheumatoid arthritis, underscore the potential benefits and risks of dual biologic therapy. Further research, including the ongoing SynBioSe-2 trial, is needed to clarify the optimal use, sequencing, and safety profile of RTX-BELI in SLE. Identifying biomarkers predictive of response may enable personalized treatment approaches, ultimately improving long-term outcomes for patients with refractory SLE.
Experiences and unmet needs of persons living with systemic lupus erythematosus in Europe: Lupus Europe's 2024 Swiss knife survey.
Cornet A, Karakikla Mitsakou Z, Andersen J … +11 more , Dyball S, Chotai R, Sluijmers A, Santos CS, Sturiene A, Scarle L, Guimarães de Oliveira D, Zuniga N, Wijsma E, Chessa E, Arnaud L
Autoimmun Rev · 2025 Jul · PMID 40403863 · Publisher ↗
Systemic lupus erythematosus (SLE) is a complex autoimmune disease with important variations in disease burden across patients and European countries. In response to previous surveys revealing the burden of SLE on patien...
Systemic lupus erythematosus (SLE) is a complex autoimmune disease with important variations in disease burden across patients and European countries. In response to previous surveys revealing the burden of SLE on patients, Lupus Europe conducted the 2024 'Swiss Knife' survey to further investigate disease burden, treatment goals, and patient-physician interactions in European patients living with lupus. Between April and May 2024, 4525 patients with self-reported physician-confirmed SLE across 36 European countries participated in an anonymous online study. Descriptive statistics were utilized to analyze responses related to SLE symptoms, treatment satisfaction, and unmet needs. Results indicated that fatigue (84.9 %), joint pain (72.8 %), and muscle pain (62.6 %) were the most prevalent symptoms, with fatigue notably under-addressed in treatment plans. The mean lupus burden score was high at 6.94 (SD: 1.95) on the 0-10 scale, highlighting a significant impact on quality of life, particularly in terms of fatigue and physical consequences. Notably, only 7.9 % of participants reported no disease flares in the past five years, contrasting with previous literature on remission rates. In terms of treatment goals, patients favored achieving low disease activity or remission without treatment, while satisfaction with current therapies was moderate, with 67.5 % expressing contentment but many indicating unmet needs, particularly regarding fatigue management and access to non-pharmacological therapies. The findings of Lupus Europe's 2024 Swiss Knife study underscore the necessity for improved communication between patients and healthcare professionals and the integration of patient-centered strategies to optimize SLE management and enhance quality of life across Europe.
Integrating network pharmacology and experimental validation to advance psoriasis treatment: Multi-target mechanistic elucidation of medicinal herbs and natural compounds.
Jo HG, Seo J, Jang B … +5 more , Kim Y, Kim H, Baek E, Park SY, Lee D
Autoimmun Rev · 2025 Jul · PMID 40381707 · Publisher ↗
BACKGROUND: Psoriasis, a chronic immune-mediated inflammatory disease (IMID), presents significant therapeutic challenges, necessitating exploration of alternative treatments like medicinal herbs (MH) and natural compoun...
BACKGROUND: Psoriasis, a chronic immune-mediated inflammatory disease (IMID), presents significant therapeutic challenges, necessitating exploration of alternative treatments like medicinal herbs (MH) and natural compounds (NC). Network pharmacology offers predictive insights, yet a systematic evaluation connecting these predictions with experimental validation outcomes specifically for MH/NC in psoriasis is lacking. This review specifically fills this gap by comprehensively integrating and analyzing studies that combine network pharmacology predictions with subsequent experimental validation. METHODS: A systematic literature search identified 44 studies employing both network pharmacology and in vitro or in vivo experimental methods for MH/NC targeting psoriasis. This review provides a systematic analysis of the specific network pharmacology platforms, predicted targets/pathways, in vivo and in vitro experimental validation models, and key biomarker changes reported across these integrated studies. Methodological approaches and the consistency between predictions and empirical findings were critically evaluated. RESULTS: This first comprehensive analysis reveals that network pharmacology predictions regarding MH/NC mechanisms in psoriasis are frequently corroborated by experimental data. Key signaling pathways, including the IL-17/IL-23 axis, MAPK, and NF-κB, emerge as consistently predicted and experimentally validated targets across diverse natural products. The review maps the specific network pharmacology tools and experimental designs utilized, establishing a methodological benchmark for the field and highlighting the successful synergy between computational prediction and empirical verification. CONCLUSION: By systematically integrating and critically assessing the linkage between network pharmacology predictions and experimental validation for MH/NC in psoriasis, this review offers a unique clarification of the current, validated state-of-the-art, differentiating it from previous literature. It confirms network pharmacology's predictive power for natural products, identifies robustly validated therapeutic pathways, and provides a crucial benchmark, offering data-driven insights for future research into artificial intelligence-enhanced natural product-based therapies for psoriasis and other IMIDs.
New thoughts on the intestinal microbiome-B cell-IgA axis and therapies in IgA nephropathy.
Dang S, Zhang X, Zhang Y … +1 more , Zhang H
Autoimmun Rev · 2025 Jul · PMID 40360014 · Publisher ↗
IgA nephropathy (IgAN), as the most common chronic glomerulonephritis worldwide, is often triggered by mucosal infections and follows a chronic progression, with the majority of patients ultimately progressing to end-sta...
IgA nephropathy (IgAN), as the most common chronic glomerulonephritis worldwide, is often triggered by mucosal infections and follows a chronic progression, with the majority of patients ultimately progressing to end-stage renal disease (ESRD) during their lifetimes. Since the mystery of its complete pathogenesis has not been fully solved, the resulting lack of effective early diagnosis and treatment greatly affects the prognosis of patients. Given the well-defined pathological feature of IgA deposition in the mesangial region, the source and role of pathogenic IgA has been focused on. Starting from the microbiology and immunity of the gut, we systematically review both the physiological and the pathological process of microbiome-B cell-IgA axis, from microbial-induced IgA production to the role of IgA in the intestinal immune milieu, and ultimately end up with the various aspects of microbiome-B cell-IgA axis in the pathogenesis of IgAN as well as the corresponding therapeutic initiatives available. Our retrospective review helps researchers to systematically understand the complex role between intestinal flora dysbiosis and pathogenic IgA in IgAN. This understanding provides a foundation for in-depth explorations to uncover more detailed pathogenic mechanisms and to develop more precise and effective diagnostic and therapeutic approaches.
Safety of biologics in patients with autoimmune rheumatic diseases during pregnancy: Systematic review and meta-analysis.
Li S, Liu H, Zeng S … +4 more , Xie J, Li Z, Yang Y, Chuan J
Autoimmun Rev · 2025 Jul · PMID 40339681 · Publisher ↗
BACKGROUND: Patients with autoimmune rheumatic diseases (ARDs) face the dual challenge of controlling disease activity while ensuring fetal safety during pregnancy. Biologics are increasingly used to treat ARDs, but evid...
BACKGROUND: Patients with autoimmune rheumatic diseases (ARDs) face the dual challenge of controlling disease activity while ensuring fetal safety during pregnancy. Biologics are increasingly used to treat ARDs, but evidence regarding their safety during pregnancy remains uncertain. This study aims to systematically evaluate the safety of biologics during pregnancy by performing a systematic review and meta-analysis. METHODS: A comprehensive search was conducted in major databases to identify studies involving pregnant ARDs patients treated with biologics from inception to 30th September 2024. The outcomes assessed included small for gestational age (SGA), cesarean section, preterm birth (PTB), low birth weight (LBW), gestational diabetes mellitus (GDM), pre-eclampsia, gestational hypertension, severe maternal infection, birth defects (BD), and a composite outcome of fetal miscarriage or death. RESULTS: A total of 40 studies involving 11,712 patients were included. The pooled prevalence of adverse pregnancy outcomes (APOs) in patients exposed to biologics was comparable to those observed in the general ARDs population. Compared to other biologics, tumor necrosis factor inhibitors (TNFis) was associated with a significantly lower prevalence of cesarean section (26.93 % vs. 63.64 %, p = 0.01), early pregnancy loss (10.44 % vs. 18.77 %, p = 0.03), and termination of pregnancy (8.59 % vs. 16.11 %, p < 0.01). Compared to csDMARDs, biologic use during pregnancy did not significantly increase the risk of APOs. CONCLUSION: Exposure to biologics during pregnancy in ARDs patients does not significantly increase the risk of APOs, with TNFis showing a well-supported safety profile, while non-TNFi biologics may carry higher risks, requiring cautious evaluation.
Interleukin-6 in neuroimmunological disorders: Pathophysiology and therapeutic advances with satralizumab.
Li X, Zhao C
Autoimmun Rev · 2025 Jun · PMID 40324548 · Publisher ↗
Interleukin-6 (IL-6) is a multifunctional cytokine produced by various cells of the innate and adaptive immune systems. It acts as a regulatory factor in immunity, inflammation, metabolism, and cellular function in multi...
Interleukin-6 (IL-6) is a multifunctional cytokine produced by various cells of the innate and adaptive immune systems. It acts as a regulatory factor in immunity, inflammation, metabolism, and cellular function in multiple organs and systems. The functionality of IL-6 is achieved through multiple signal transduction pathways, such as the JAK/STAT and the NF-κB signaling pathways. In this review, we highlighted the inflammatory and non-inflammatory functions of IL-6, as well as the associated signaling pathways. The involvement of IL-6 in neuroimmunological disorders suggests that the interleukin-6 receptor (IL-6R) monoclonal antibody, satralizumab, is a potential therapeutic strategy. Phase III clinical trials have already validated the safety and efficiency of satralizumab in treating neuromyelitis optica spectrum disorders (NMOSD) and acetylcholine receptor (AChR) seropositive generalized myasthenia gravis (gMG). This review aims to elucidate the pathophysiological role of IL-6, and explore the clinical implications of satralizumab in neuroimmunological diseases, providing insights into its potential therapeutic applications.
Adipokines in multiple sclerosis: Immune dysregulation, neuroinflammation, and therapeutic opportunities.
Ghaffary EM, Bjørklund G, Bhat RS … +1 more , Mirmosayyeb O
Autoimmun Rev · 2025 Jul · PMID 40311722 · Publisher ↗
Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS), characterized by demyelination, neuroinflammation, and the progressive accumulation of neurologic deficits. Adipose tissue sec...
Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS), characterized by demyelination, neuroinflammation, and the progressive accumulation of neurologic deficits. Adipose tissue secretes predominantly the bioactive molecules, known as adipokines, which have drawn considerable attention for their roles in modulating immune and metabolic pathways in people with MS (PwMS). Dysregulated adipokines, such as resistin, leptin, and chemerin, induce pro-inflammatory T-cell polarization while deteriorating Blood-Brain Barrier (BBB) integrity. Adiponectin, by contrast, has both immunomodulatory and neuroprotective functions. The opposing functionality highlights the biomarker and the therapeutic potential of adipokines. Preclinical and translational findings have shed light on the role of adipokines in the pathophysiology of MS by influencing T-cell, glial, and BBB functions. In clinical settings, the assessment of adipokines can function as an indicator of prognosis and diagnosis via distinct patterns of expression. In addition, alterations to adipokine profiles through lifestyle changes and pharmaceutical treatment may complement established disease-modifying treatments (DMTs). This study has highlighted the multifaceted role of adipokines in MS management, while further studies exploring the role of adipokine-mediated immunometabolic regulation are suggested.
The emerging concept of ANCA-associated vasculitis related to inborn errors of immunity.
Triaille C, Terrier B, Hadchouel A … +3 more , Haddad E, Vaglio A, Frémond ML
Autoimmun Rev · 2025 Jun · PMID 40294837 · Publisher ↗
ANCA-associated vasculitis (AAV) is a group of rare small vessels vasculitis that preferentially affect the kidneys, lungs and upper airways. Although the detailed pathophysiology remains unclear, genetic background has...
ANCA-associated vasculitis (AAV) is a group of rare small vessels vasculitis that preferentially affect the kidneys, lungs and upper airways. Although the detailed pathophysiology remains unclear, genetic background has been shown to play a role in sporadic forms of AAV. The discovery of these susceptibility genes (and associated biological pathways) involved in AAV have shaped the current understanding of AAV pathophysiology. In addition to common genetic polymorphisms, specific rare inborn errors of immunity (IEI) have been described with a high frequency of ANCA (antineutrophil cytoplasmic antibodies) positivity and vasculitis features in young individuals (in addition to other manifestations). A systematic literature search revealed that patients with pathogenic variants in COPA, STING1, DNASE1L3, and PIK3CD are at increased risk of developing ANCA and AAV features, including alveolar hemorrhage, interstitial lung disease, pauciimmune glomerulonephritis, and upper airways involvement (septum perforation, saddle-nose deformity, chronic nasal/sinuses ulceration). Some of these IEI may also present with a mixed phenotype and/or auto-antibodies profile associating features of AAV and other autoimmune diseases (in particular systemic lupus erythematosus). Notably, a proportion of reports and series lack serological (ANCA specificity and titers) and/or histopathological data, making challenging to assess the likelihood for ANCA pathogenicity in some patients with IEI (as opposed to unspecific signs of biologic autoimmunity). This point is nonetheless essential to make appropriate therapeutic decisions. In addition, since most of the genes mentioned above are involved in the type 1 interferon signaling, the role of this pathway in AAV etiopathogenesis deserves further investigation. In this review, we will describe these IEI, their overlap with sporadic AAV, and their evocative features. Next, we will discuss how these monogenic conditions might inform our general understanding of AAV pathophysiology. We also propose some directions for future research in order to better define the link between ANCA and IEI. Finally, we will consider how making the diagnosis of an IEI in a patient with AAV features might impact individual management.
Coffee consumption and risk of multiple sclerosis: A systematic review and meta-analysis.
Amirnia M, Raeisnia K, Ashayeri H … +5 more , Hakimzadeh Z, Nasiri E, Talebi M, Sanaie S, Naseri A
Autoimmun Rev · 2025 Jun · PMID 40286889 · Publisher ↗
BACKGROUND: Multiple Sclerosis (MS) is an immune-mediated disease with miscellaneous etiological origins. Given caffeine's neuroprotective and anti-inflammatory attributes and its potential influence on MS risk, and to a...
BACKGROUND: Multiple Sclerosis (MS) is an immune-mediated disease with miscellaneous etiological origins. Given caffeine's neuroprotective and anti-inflammatory attributes and its potential influence on MS risk, and to address the conflict in the clinical evidence, this study aims to comprehensively review the existing literature on the association between coffee consumption and the risk of MS. METHODS: Following the PRISMA 2020 guidelines, a systematic search in PubMed, Scopus, Web of Science, and Embase for the studies published up to January 2024 was conducted. Studies that assessed the relationship between coffee intake and the risk of MS were included, and reviews, case reports, non-English papers, in vitro and animal studies, and conference abstracts were excluded. The risk of bias was assessed using the JBI checklists, and meta-analyses were conducted based on odds ratio (OR) using the fourth version of CMA software. RESULTS: Out of 604 initial records, 10 observational studies with 19,430 participants met the inclusion criteria. The included case-control studies showed an overall high quality. Meta-analysis revealed a reduction in MS development in coffee consumers both before (OR: 0.66; 95 % CI: 0.49-0.90; p-value: 0.008; I: 89.65 %; p-value for heterogeneity<0.001) and after adjustment for possible confounders (adjusted OR: 0.42; 95 % CI: 0.20-0.90; p-value: 0.025; I: 89.65 l; p-value for heterogeneity<0.001). CONCLUSION: Coffee consumption, may decrease the risk of MS; however, further well-designed prospective studies are required to ascertain this association. PROSPERO registration number: CRD42023484298.
Rebalancing redox homeostasis: A pivotal regulator of the cGAS-STING pathway in autoimmune diseases.
Zhao Y, Xu T, Wu Z … +2 more , Li N, Liang Q
Autoimmun Rev · 2025 May · PMID 40286888 · Publisher ↗
Autoimmune diseases (ADs) arise from the breakdown of immune tolerance to self-antigens, leading to pathological tissue damage. Proinflammatory cytokine overproduction disrupts redox homeostasis across diverse cell popul...
Autoimmune diseases (ADs) arise from the breakdown of immune tolerance to self-antigens, leading to pathological tissue damage. Proinflammatory cytokine overproduction disrupts redox homeostasis across diverse cell populations, generating oxidative stress that induces DNA damage through multiple mechanisms. Oxidative stress-induced alterations in membrane permeability and DNA damage can lead to the recognition of double-stranded DNA (dsDNA), mitochondrial DNA (mtDNA) and micronuclei-DNA (MN-DNA) by DNA sensors, thereby initiating activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. While previous reviews have characterized cGAS-STING activation in autoimmunity, the reciprocal regulation between redox homeostasis and cGAS-STING activation remains insufficiently defined. This narrative review examines oxidative stress-mediated DNA damage as a critical driver of pathological cGAS-STING signaling and delineates molecular mechanisms linking redox homeostasis to autoimmune pathogenesis. Furthermore, we propose therapeutic strategies that combine redox restoration with the attenuation of aberrant cGAS-STING activation, thereby establishing a mechanistic foundation for precision interventions in autoimmune disorders. METHODS: The manuscript is formatted as a narrative review. We conducted a comprehensive search strategy using electronic databases such as PubMed, Google Scholar and Web of Science. Various keywords were used, such as "cGAS-STING," "Redox homeostasis," "Oxidative stress," "pentose phosphate pathway," "Ferroptosis," "mtDNA," "dsDNA," "DNA damage," "Micronuclei," "Reactive oxygen species," "Reactive nitrogen species," "Nanomaterial," "Autoimmune disease," "Systemic lupus erythematosus," "Type 1 diabetes," "Rheumatoid arthritis," "Multiple sclerosis," "Experimental autoimmune encephalomyelitis," "Psoriasis," etc. The titles and abstracts were reviewed for inclusion into this review. After removing duplicates and irrelevant studies, 174 articles met inclusion criteria (original research, English language).
The role of double-negative B cells in the pathogenesis of systemic lupus erythematosus.
Qiu X, Wen R, Wu F … +10 more , Mao J, Azad T, Wang Y, Zhu J, Zhou X, Xie H, Hong K, Li B, Zhang L, Wen C
Autoimmun Rev · 2025 Jun · PMID 40274006 · Publisher ↗
B cells are essential to the pathophysiology of systemic lupus erythematosus (SLE), a chronic autoimmune illness. IgD-CD27-double negative B cells (DNB cells) are one of the aberrant B cell subsets linked to SLE that hav...
B cells are essential to the pathophysiology of systemic lupus erythematosus (SLE), a chronic autoimmune illness. IgD-CD27-double negative B cells (DNB cells) are one of the aberrant B cell subsets linked to SLE that have attracted much scientific interest. There is growing evidence that DNB cells play a significant role in the development of the disease and are strongly linked to the activity of lupus. These cells play a pivotal role in the pathogenesis of SLE by producing a diverse array of autoantibodies, which form immune complexes that drive target organ damage. A comprehensive understanding of SLE pathophysiology necessitates in-depth investigation into DNB cells, not only to elucidate their mechanistic contributions but also to uncover novel therapeutic strategies. According to available data, treatments that target B cells have proven effective in managing SLE; nevertheless, a significant breakthrough in precision medicine for SLE may come from targeting DNB cells specifically. Despite growing interest in DNB cells, their precise characteristics, developmental trajectories, and regulatory mechanisms remain incompletely defined, posing significant challenges to the field. A comprehensive investigation of the regulatory mechanisms governing DNB cell differentiation and expansion in SLE may facilitate novel therapeutic discoveries. This review aims to provide an updated synthesis of current research on DNB cells, with a focus on their origins, developmental trajectories in SLE, and potential as precision therapeutic targets.
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