Autoimmunity Reviews[JOURNAL]
Sun
200 papers
Itaconate: A key regulator of immune responses and potential therapeutic target for autoimmune and inflammatory diseases.
Liu Y, Jiang X, Zhuang S … +4 more , Zhu L, Zhu B, Rui K, Tian J
Autoimmun Rev · 2025 Sep · PMID 40683614 · Publisher ↗
Itaconate, a metabolite of the tricarboxylic acid cycle (TAC), has gained increasing attention in recent years due to its anti-inflammatory and immunomodulatory properties. It plays a crucial role in immune regulation by...
Itaconate, a metabolite of the tricarboxylic acid cycle (TAC), has gained increasing attention in recent years due to its anti-inflammatory and immunomodulatory properties. It plays a crucial role in immune regulation by modulating signal transduction and posttranslational modification. Itaconate is derived from cis-aconitate decarboxylation and is produced by cis-aconitate decarboxylase (ACOD1) in the mitochondria. During cellular stress conditions, itaconate rapidly accumulates in myeloid cells. Recent studies have demonstrated that itaconate plays a pivotal role in modulating both innate and adaptive immune responses. Moreover, itaconate regulates the differentiation and function of innate immune and lymphoid cells, which is implicated in the pathogenesis of autoimmune diseases. In this review, we aim to explore the recent advancements in comprehending the functional regulation and mechanisms of itaconate in various populations of innate immune and lymphoid cells, as well as its immunomodulatory effects in the development of autoimmune diseases. In addition, we highlight the potential therapeutic applications of itaconate and its derivatives in autoimmune diseases.
Chronic inflammation in Long COVID relationship to autoimmune diseases.
Chen K, Wang Z, Li J … +6 more , Xu Y, Gu S, Li H, Li J, Zhang Y, Mao N
Autoimmun Rev · 2025 Sep · PMID 40683613 · Publisher ↗
The new coronavirus pandemic has been ongoing for nearly five years. In addition to the severe symptoms in the acute phase, it is accompanied by long-term complications and sequelae involving the respiratory, neurologica...
The new coronavirus pandemic has been ongoing for nearly five years. In addition to the severe symptoms in the acute phase, it is accompanied by long-term complications and sequelae involving the respiratory, neurological, immune, circulatory, and gastrointestinal systems for several months or even years, which is called the Long COVID. Many studies have suggested that systemic chronic inflammation caused by residual viral components may be one of the pathophysiologic mechanisms of Long COVID. In this paper, we will review the autoimmune diseases caused by chronic inflammation. In particular, cytokine storminess, pro-inflammatory responses of inflammatory vesicles, mast cell activation syndrome, changes in the gut microbiota, molecular mimicry, reactivation of latent viruses, and coagulation abnormalities are among the pathways that contribute to autoimmune diseases, including Systemic Lupus Erythematosus, Guillain-Barré syndrome, rheumatoid arthritis. We intervene in the treatment of the disease with probiotics, immunoglobulins, the RECOVER clinical trial model, and immunomodulatory drugs. The aim is to enhance understanding of the pathophysiological mechanism of Long COVID and to provide a reference for the immunotherapy of patients.
The role of γδ T cells and CAR-γδ T cell therapy in autoimmune diseases.
Wang T, Wang H, Lv R … +3 more , Wen C, Wang M, Huang L
Autoimmun Rev · 2025 Sep · PMID 40681068 · Publisher ↗
Autoimmune diseases represent a major global health challenge, imposing substantial economic, social, and personal burdens on human society. γδ T lymphocytes are a unique T cell subset that bridges innate and adaptive im...
Autoimmune diseases represent a major global health challenge, imposing substantial economic, social, and personal burdens on human society. γδ T lymphocytes are a unique T cell subset that bridges innate and adaptive immunity, demonstrating remarkable characteristics in immune regulation and inflammatory modulation. In this context, Chimeric Antigen Receptor (CAR)-γδ T cell therapy emerges as a promising immunotherapeutic strategy with transformative potential in addressing autoimmune disorders. This review comprehensively explores the multifaceted roles of γδ T lymphocytes in autoimmune pathogenesis, highlighting their distinctive functions and properties. It discusses the potential and advantages of applying γδ T cells to CAR-T cell therapy, elucidating the prospects of treating autoimmune diseases through CAR-γδ T cell therapy in the future.
Authors' response to "comment on 'systemic lupus erythematosus and male reproductive health: A systematic review and meta-analysis'".
Zhu Q, Li X, Zhao T
Autoimmun Rev · 2025 Sep · PMID 40675353 · Publisher ↗
Abstract loading — click title to view on PubMed.
The FOXO1-SIRT1 axis in ankylosing spondylitis: A cross-platform regulator linking immunometabolism, oxidative stress, and bone remodeling.
Zhang X, Jia L, Lin X … +1 more , Zhou L
Autoimmun Rev · 2025 Sep · PMID 40669681 · Publisher ↗
Ankylosing spondylitis (AS) is a chronic immune-mediated disorder defined by the paradoxical coupling of inflammatory bone erosion and ectopic new bone formation. Recent studies implicate the Forkhead box O1 (FOXO1)-Sirt...
Ankylosing spondylitis (AS) is a chronic immune-mediated disorder defined by the paradoxical coupling of inflammatory bone erosion and ectopic new bone formation. Recent studies implicate the Forkhead box O1 (FOXO1)-Sirtuin 1 (SIRT1) signaling axis as a systems-level regulator integrating immune metabolism, redox balance, and skeletal remodeling. FOXO1 and SIRT1 cooperatively regulate immune tolerance, redox balance, and skeletal homeostasis via transcriptional, epigenetic, and metabolic pathways. This review delineates the cross-platform roles of the FOXO1-SIRT1 axis across three interrelated modules: regulation of immune cell metabolism and polarization; redox sensing and organelle quality control via autophagy and mitophagy; and coordination of osteoblast - osteoclast dynamics in inflammatory microenvironments. Dysregulation of this axis disrupts immuno-metabolic equilibrium and promotes pathological ossification, contributing to the dual pathology of AS. We further discuss emerging therapeutic strategies - ranging from SIRT1 activators and anti -Interleukin-17 A (IL-17 A) biologics to histone deacetylase inhibitors - that converge mechanistically on FOXO1-SIRT1 signaling. These translational approaches underscore the axis's potential as a cross-domain integrator of immune and skeletal homeostasis, and as a promising target for precision intervention in AS.
Remission and low disease activity definitions in adult idiopathic inflammatory myopathies: A narrative review by myositis clinical trials consortium (MCTC).
Pongtarakulpanit N, Keret S, Kothari V … +16 more , Bozán F, Kavadichanda C, Yoshida A, Leclair V, Bishnoi A, Ardalan K, Conticini E, Lan TY, Landon-Cardinal O, Tang IYK, Rosina S, Yi BY, Lilleker JB, Dourado E, Gandiga PC, Aggarwal R
Autoimmun Rev · 2025 Sep · PMID 40669680 · Publisher ↗
Idiopathic inflammatory myopathies (IIM) are a heterogeneous group of rare systemic autoimmune rheumatic diseases. Despite advances in treatment, the definition of remission and low disease activity (LDA) in IIM remains...
Idiopathic inflammatory myopathies (IIM) are a heterogeneous group of rare systemic autoimmune rheumatic diseases. Despite advances in treatment, the definition of remission and low disease activity (LDA) in IIM remains inconsistent and lacks consensus and validation. This review summarizes existing published definitions, achievement rates, and predictive factors of remission/LDA in adult IIM, focusing on dermatomyositis (DM), polymyositis (PM), anti-synthetase syndrome (ASyS), and immune-mediated necrotizing myopathies (IMNM). Our literature review revealed a wide variability in remission definitions, incorporating physician assessment, muscle strength, laboratory normalization, and medication tapering or discontinuation. Some studies defined "remission on medication", while others required complete treatment cessation. Most definitions required a minimum duration of six months. Organ-specific remission (including for the skin, lung, and muscle domains) was inconsistently addressed. LDA has been less extensively studied in IIM, with the myositis disease activity assessment visual analog scales (MYOACT) being the only measure applied to DM. Remission rates varied widely, with stricter criteria yielding lower rates. Factors associated with remission included younger age, early immunosuppressive treatment, non-severe muscle involvement, the absence of myositis-specific autoantibodies (MSA), although some studies reported positivity for certain MSA were associated with remission. Conversely, remission was less likely for patients with PM, overlap myositis, and those positive for anti-TIF1-γ or Ku autoantibodies. Standardized remission criteria incorporating physician assessment, patient assessment, organ-specific parameters, laboratory assessments, and sustained remission duration are essential for harmonizing clinical and research evaluations in IIM. Establishing uniform definitions will improve therapeutic outcome assessments and facilitate meaningful comparisons in clinical trials and real-world practice.
Glycometabolic reprogramming of immune cells in autoimmune diseases.
Lin J, Yang F, Zheng Y … +3 more , Wang X, Fan X, Yang L
Autoimmun Rev · 2025 Sep · PMID 40669679 · Publisher ↗
Autoimmune diseases (ADs) are a classification of disorders that occur owing to the breakdown of immunological tolerance to self-antigens, leading to an immune response to these antigens and associated bodily harm. The p...
Autoimmune diseases (ADs) are a classification of disorders that occur owing to the breakdown of immunological tolerance to self-antigens, leading to an immune response to these antigens and associated bodily harm. The pathogenesis and etiology of these diseases remain unclear. A growing body of research indicates that metabolic reprogramming of immune cells is crucial for immunological control. In particular, glycolysis, a crucial metabolic process in cells, is reconfigured to influence the phenotypic and function of immune cells, therefore playing a role in the onset and progression of ADs. This review elaborates on the involvement of glycometabolic reprogramming in ADs and explores the function of glycometabolic reprogramming in immune cells throughout disease progression. Furthermore, we examine the principal targets implicated and their influence on disease advancement. Finally, we provide a brief summary and outlook of studies related to glycometabolic reprogramming of immune cells in ADs, aiming to guide therapeutic strategies for these diseases.
Myasthenia gravis with antibodies against the AChR, current knowledge on pathophysiology and an update on treatment strategies with special focus on targeting plasma cells.
Mané-Damas M, Schöttler AK, Marcuse F … +11 more , Molenaar PC, Mohile T, Hoeijmakers JGJ, Hochstenbag M, Damoiseaux J, Maessen JG, Abdul-Hamid M, Zur Hausen A, de Baets MH, Losen M, Martinez-Martinez P
Autoimmun Rev · 2025 Sep · PMID 40651620 · Publisher ↗
Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder where the neuromuscular transmission is impaired, causing symptoms of skeletal muscle weakness and fatigue. The presence of autoantibodies against the mu...
Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder where the neuromuscular transmission is impaired, causing symptoms of skeletal muscle weakness and fatigue. The presence of autoantibodies against the muscle nicotinic acetylcholine receptor (AChR) is the most prevalent cause of MG. Abnormalities in the thymus are common in AChR-MG, and thymectomy has proven to be therapeutically beneficial. Up to 30 % of AChR-MG patients have also thymoma. Moreover, patients with thymoma without MG are more prompt to develop MG compared to the general population. Autoantibodies in AChR-MG damage the postsynaptic membrane of the neuromuscular junction (NMJ) and cause muscle weakness by impairing synaptic transmission because of the depletion of the AChRs and destruction of the NMJ. The pathogenic autoantibody levels vary greatly between patients. In contrast, in individual patients changes in autoantibody levels correlate well with disease severity. A small selection of patients has been used to exemplify the individual relationship between autoantibody levels and disease progression. The study of the effector functions of the autoantibodies and the compensatory mechanisms at the NMJ are important to select the best treatment strategy for each patient. Even though classical immunomodulatory treatments are effective in many patients, around 10-20 % of patients do not respond to current therapies. This may be attributed to the production of autoantibodies by different circulating cells including mature B and long-lived plasma cells, which are resistant to most commonly used immunosuppressive drugs. Hence, novel therapies specifically targeting plasma cells might be a suitable therapeutic approach for selected refractory patients.
The roles of transient receptor potential vanilloid in autoimmune diseases.
Xiao Y, Xin Y, Shen K … +2 more , Yang M, Wu H
Autoimmun Rev · 2025 Sep · PMID 40639777 · Publisher ↗
The transient receptor potential vanilloid (TRPV) is a family of tetrameric cation channels, expressed in various tissues and cell types. It includes thermosensitive isoforms (TRPV1-4) and calcium-permeable members (TRPV...
The transient receptor potential vanilloid (TRPV) is a family of tetrameric cation channels, expressed in various tissues and cell types. It includes thermosensitive isoforms (TRPV1-4) and calcium-permeable members (TRPV5-6). In the context of autoimmune diseases, TRPV channels have been firmly established as pivotal regulators that bridge changes in the cellular environment to the immune system. Originally identified for their roles in thermosensation and nociception, these polymodal sensors have now emerged as crucial determinants of immune cell function. They are capable of converting chemical signals, temperature fluctuations, and mechanical forces into calcium-mediated signal transduction pathways. Mounting evidence indicates that dysregulated TRPV channel activity leads to pathological calcium influx, triggering a signaling cascade that reprograms the functions of key immune cells and modulates pain and itch signaling through neuroimmune crosstalk. These cascades amplify inflammatory responses, exacerbate autoimmune pathology, promote inflammatory cytokine release, and modulate pain/itch signaling via neuroimmune crosstalk. Specifically, these mechanisms are instrumental in the progression including autoimmune disorders, such as rheumatoid arthritis (RA), inflammatory bowel disease (IBD), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), multiple sclerosis (MS), psoriasis, and atopic dermatitis (AD). Novel therapeutic strategies are emerging, aiming to modulate TRPV activity in autoimmune conditions. Approaches include suppressing hyperactive channels and leveraging their immunoregulatory potential. Promising preclinical results have highlighted that TRPV channels exhibit dual translational potential in mechanistic research of autoimmune diseases, integrating precise targeting with dynamic monitoring capabilities. However, translating these findings into clinical applications faces significant challenges, including differential effects on neuronal and immune signaling, as well as systemic side effects caused by disruptions to physiological homeostasis. This narrative review discuss how TRPV channel signaling has enhanced our understanding of autoimmune disease initiation. By dissecting how TRPV-mediated immune dysregulation drives pathological immune responses, we seek to offer novel mechanistic insights to inform the development of more effective and comprehensive treatment strategies for autoimmune diseases.
Proportion of circulating T follicular helper cells in peripheral blood of systemic lupus erythematosus patients: A systematic review and meta-analysis.
Feng F, Wu Z, Xu H … +2 more , Li Y, Zhang S
Autoimmun Rev · 2025 Sep · PMID 40639776 · Publisher ↗
OBJECTIVES: Dysregulation of circulating follicular helper T (cTfh) cells plays a key role in the breakdown of immune tolerance and the pathogenesis of antibody-mediated autoimmune diseases, including systemic lupus eryt...
OBJECTIVES: Dysregulation of circulating follicular helper T (cTfh) cells plays a key role in the breakdown of immune tolerance and the pathogenesis of antibody-mediated autoimmune diseases, including systemic lupus erythematosus (SLE). This study aims to evaluate the proportions of cTfh cells and their potential pathogenic mechanisms in the peripheral blood of SLE patients through a systematic review and meta-analysis. METHODS: Systematic search and review were conducted across PubMed, Cochrane Library, EMBASE, and Web of Science to identify relevant studies. A meta-analysis was performed to compare the proportions of cTfh cells and their subsets between SLE patients and healthy controls (HC). Subgroup analyses were conducted based on the markers used for defining cTfh cells and geographical regions. RESULTS: The meta-analysis revealed a significantly higher proportion of cTfh cells in SLE patients compared to HC (SMD 0.904, [0.620, 1.188], p < 0.01). Subgroup analyses showed a consistent increase in cTfh cells in SLE across different markers. Geographically, both Asian (SMD 1.005, [0.608, 1.402], p < 0.01) and non-Asian populations (SMD 0.708, [0.428, 0.988], p < 0.01) demonstrated elevated cTfh cell proportions in SLE. A trend toward a decrease in Tfh1 cells and an increase in Tfh17 cells was observed, though neither reached statistical significance. CONCLUSION: Our study demonstrates that cTfh cells proportions are significantly elevated in SLE patients, supporting their role in the pathogenesis of SLE. These findings suggest that cTfh cells could serve as potential biomarkers for SLE and therapeutic targets for treatment.
Trends in rheumatoid arthritis among U.S. women aged 20 to 44 years, 2001 to 2023.
Zhao Y, Cui W, Han Y … +1 more , Chang M
Autoimmun Rev · 2025 Aug · PMID 40633796 · Publisher ↗
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Combination targeted therapy with two biologic/targeted synthetic DMARDs in 1200 patients with immune mediated inflammatory diseases. A systematic literature review for current landscape in safety and efficacy.
Lignou AZ, Vassilakis KD, Baraliakos X … +3 more , Sfikakis PP, Gottenberg JE, Fragoulis GE
Autoimmun Rev · 2025 Sep · PMID 40633795 · Publisher ↗
BACKGROUND: Immune-mediated inflammatory diseases (IMID) include rheumatoid arthritis (RA), psoriatic arthritis (PsA), axial spondyloarthritis (axSpA), Crohn's disease (CD), ulcerative colitis (UC), and psoriasis (PsO)....
BACKGROUND: Immune-mediated inflammatory diseases (IMID) include rheumatoid arthritis (RA), psoriatic arthritis (PsA), axial spondyloarthritis (axSpA), Crohn's disease (CD), ulcerative colitis (UC), and psoriasis (PsO). While biologic (b) and targeted synthetic (ts) DMARDs are effective, nearly 60 % of patients fail to achieve low disease activity status. Combination targeted therapy (CTT) using concomitantly two different b- or ts-DMARDs has been explored, but results on safety and efficacy are unclear. OBJECTIVE: To systematically review the literature on CTT in IMID. METHODS: Following the PICO framework, we included literature of adult patients (≥18 years) with IMID receiving CTT. Three databases (PubMed, Scopus, Epistemonikos) were searched up to June 2024. Studies in non-English, pediatric populations, and non-approved treatments were excluded. Risk of bias was assessed using approved tools. RESULTS: Of 2038 records, 70 studies (6 RCTs, 11 cohorts, 22 case series, 31 case reports) involving 1200 patients were analyzed. About 75 % of them demonstrated low risk of bias. The most studied combinations were TNFi+IL/23i, JAKi+bDMARDs, and vedolizumab+TNFi. Approximately 40-60 % of patients with PsA, axSpA, and IBD with refractory disease improved with TNFi+IL/23i CTT. About half of patients with inflammatory arthritis and up to 80 % of IBD cases benefited with JAKi+bDMARD CTT, whereas favorable outcomes were observed in 30-50 % of IBD patients following Vedolizumab+TNFi CTT. Safety profiles were generally acceptable, without emerging signals so far. CONCLUSION: CTT benefits about half of refractory IMID patients, particularly TNFi/IL-23i, JAKi/bDMARD, and vedolizumab/TNFi combinations, without raising significant safety issues. Further research is needed to clarify safety and efficacy across diseases.
Glucagon-Like Peptide-1 (GLP-1) receptor agonists in rheumatology: A review of current evidence and future directions.
Bilgin E, Venerito V, Bogdanos DP
Autoimmun Rev · 2025 Aug · PMID 40617296 · Publisher ↗
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have improved the management of type 2 diabetes and obesity. Increasing evidence suggests their potential therapeutic role in rheumatic and musculoskeletal diseases,...
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have improved the management of type 2 diabetes and obesity. Increasing evidence suggests their potential therapeutic role in rheumatic and musculoskeletal diseases, yet their precise mechanisms and clinical implications remain under investigation. This scoping review evaluates the current evidence on GLP-1 RAs in inflammatory arthritis, osteoarthritis, systemic autoimmune diseases, and other rheumatic conditions. This systematic literature search followed PRISMA-ScR guidelines and identified 52 studies and seven clinical trials from Scopus, PubMed, and ClinicalTrials.gov. Although most of the included studies had a risk of bias, the findings suggest that GLP-1 RAs may influence inflammatory pathways, oxidative stress, and immune regulation in conditions such as rheumatoid arthritis (RA), psoriatic arthritis (PsA), systemic lupus erythematosus (SLE), osteoarthritis (OA), and gout. In RA and PsA, GLP-1 RAs have demonstrated potential disease-modifying effects, reducing inflammatory cytokine expression and improving metabolic parameters; however, their clinical impact remains partially linked to weight loss. Studies on OA indicate chondroprotective and anti-inflammatory properties, yet their effect on disease progression remains inconclusive. Additionally, GLP-1 RAs have been associated with cardiovascular and renal benefits in SLE, though concerns about autoimmune activation persist. Despite promising findings, several challenges remain, including heterogeneous clinical responses, the need for head-to-head comparisons with standard rheumatologic therapies, and a lack of long-term safety data in autoimmune conditions. Drug-induced autoimmune phenomena, cost considerations, and accessibility limitations must be addressed. Future research should focus on distinguishing between metabolic and direct immunomodulatory effects, optimizing combination therapies, and evaluating safety concerns. GLP-1 RAs hold potential as a novel therapeutic approach in rheumatology, but further well-designed randomized controlled trials are essential to establish their clinical role.
Epidemiological patterns and in-hospital mortality in ANCA-associated vasculitis: Insights from Spain's National Health Data (2016-2022).
Cordero-Pérez FJ, Martínez-Rodríguez P, Arribas-Pérez L … +8 more , Puertas-Miranda D, Pires-Baltazar CR, Salcedo-Martín L, Sánchez-Villoria JA, Díaz-Ávila EG, Ternavasio-De La Vega HG, Marcos M, Chamorro AJ
Autoimmun Rev · 2025 Aug · PMID 40602701 · Publisher ↗
BACKGROUND: ANCA-associated vasculitis (AAV), including granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA), is a systemic autoimmune disease....
BACKGROUND: ANCA-associated vasculitis (AAV), including granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA), is a systemic autoimmune disease. This study represents the first large-scale analysis of AAV hospitalisation rates and in-hospital mortality trends in Spain. METHODS: A retrospective longitudinal analysis of AAV-related hospital admissions between 2016 and 2022 was conducted using the ICD-10 codes from the Minimum Basic Dataset (MBDS) of the Spanish National Health System. Statistical analyses were performed, including odds ratios, Student's t-tests, and Mantel-Haenszel trend tests. RESULTS: Among 5753 AAV episodes, GPA was the most frequent subtype (53.9 %), followed by MPA (31.5 %) and EGPA (14.6 %). AAV episodes were more frequent in older patients (> 65 years) than in other hospital episodes (62.9 % vs. 38.9 %; OR: 2.66, 95 %CI: 2.51-2.80; P < 0.001). Larger hospitals accounted for more AAV episodes, longer hospital stays, and higher costs. MPA had the highest mortality rate (7.2 % vs. 4.9 %; OR: 1.52, 95 % CI: 1.27-1.79; P < 0.001), particularly in patients over 65 years (83.1 % vs. 61.8 %; OR: 3.04, 95 % CI: 2.47-3.75; P < 0.001) compared with the other AAV. In the GPA group, renal involvement significantly increased mortality compared to GPA cases without renal involvement (6.6 % vs. 4.6 %; OR: 1.46, 95 % CI: 1.16-1.83; P = 0.011). Notably, the relative risk of AAV-related deaths increased over the study period (Z = 2.77, P < 0.01). CONCLUSION: AAV, particularly MPA, is associated with increased hospital mortality, particularly among older adults and patients with renal involvement.
The efficacy and safety of monoclonal anti-TNF antibodies in the treatment of vascular Behçet's syndrome: A systematic review and meta-analysis.
Liu Y, Wu J, Ao Y … +7 more , Li L, Wang X, Zhang M, Yu X, Sun L, Liu J, Zheng W
Autoimmun Rev · 2025 Aug · PMID 40602700 · Publisher ↗
OBJECTIVES: This study is the first meta-analysis to evaluate the efficacy and safety of monoclonal anti-TNF antibodies in patients with vascular Behçet's syndrome (VBS). METHODS: A comprehensive literature search was co...
OBJECTIVES: This study is the first meta-analysis to evaluate the efficacy and safety of monoclonal anti-TNF antibodies in patients with vascular Behçet's syndrome (VBS). METHODS: A comprehensive literature search was conducted on PubMed, Embase, Cochrane Library, Medline Complete, and Web of Science. Pooled estimates of clinical response including complete response (CR) and partial response (PR), were calculated at 3, 6, and 12 months. Subgroup analyses were performed based on the specific monoclonal anti-TNF antibodies used. Additionally, pooled proportions of imaging response before and after 6 months were assessed. RESULTS: Twelve studies involving 297 patients were included. The pooled proportions of clinical CR were 64.1 % (95 %CI 28.7-93.9 %), 89.1 % (95 %CI 72.4-98.6 %), and 94.5 % (95 %CI 82.5-99.8 %) at 3, 6, and 12 months, respectively. Imaging response was achieved in 92.9 % (95 %CI 77.2-100 %) of patients within 6 months and 92.5 % (95 %CI 74.8-99.9 %) after 6 months. During follow-up, 26 patients experienced a relapse while on monoclonal anti-TNF antibodies treatment. Of the 43 patients who discontinued therapy due to response, 28 % (n = 12) experienced a relapse. Adverse events (AEs) were reported in 10 studies involving 42 patients, with 31 patients experiencing severe AEs, including 5 deaths. CONCLUSIONS: Monoclonal anti-TNF antibodies are an effective treatment for VBS, demonstrating significant clinical and radiological efficacy with a favorable safety profile. Prevention of relapses and control of disease progression remain critical objectives in VBS management. Further validation of their efficacy through randomized controlled trials (RCTs) stratified by arterial and venous involvement is warranted to strengthen the evidence base and optimize therapeutic strategies.
Infectious agents in dilated cardiomyopathy: Genetic interactions, autoimmunity, mechanisms, and therapeutic approaches.
Zhang J, Zhan H, Xu H … +8 more , Wang R, Li Z, Feng F, Wu H, Xu Z, Wang S, Guo Y, Li Y
Autoimmun Rev · 2025 Aug · PMID 40562294 · Publisher ↗
Dilated cardiomyopathy (DCM) is a heterogeneous myocardial disorder characterized by left ventricular dilation and systolic dysfunction in the absence of ischemic, hypertensive, or valvular heart disease. Although its pr...
Dilated cardiomyopathy (DCM) is a heterogeneous myocardial disorder characterized by left ventricular dilation and systolic dysfunction in the absence of ischemic, hypertensive, or valvular heart disease. Although its precise etiology remains unclear, it is widely recognized as a multifactorial disease arising from complex interactions between genetic predisposition and environmental triggers. Among these, infectious agents have been implicated in the pathogenesis of various subtypes, particularly inflammatory and idiopathic DCM. These agents can contribute to disease onset and progression through direct cardiomyocyte injury, immune-mediated chronic inflammation, and other yet-to-be-defined mechanisms. Infection-driven autoimmune activation is another potential key contributor to DCM, potentially linking infectious exposure to sustained myocardial damage. However, the precise role of various infectious agents in DCM initiation and progression, as well as their interactions with genetic predisposition and autoimmune activation, is inadequately understood. Improving understanding of infection-related etiologies could facilitate development of targeted therapeutic strategies; however, significant challenges persist in identifying causative and novel pathogens, and translating this into clinical practice. Therefore, this review explores the complex interactions between infectious agents, genetic predisposition, and autoimmune responses in DCM pathogenesis. We summarize current evidence on the role of infectious agents in DCM and emerging therapeutic strategies aimed at treating infection-related DCM. Finally, we outline future research directions to advance understanding of infection-associated DCM and improve patient outcomes. We reveal that a deeper understanding of host-microbe interactions, immune pathways, and genetic predisposition is essential for advancing DCM research. Furthermore, integrating genomics, metagenomics, and antibody and immunological profiling is crucial for developing personalized therapeutic strategies for this complex disease.
Mesenchymal stem cell in immunomodulation of dendritic cells: Implications for inflammatory bowel disease therapy.
Song D, He C, Ocansey DKW … +3 more , Wang B, Wu Y, Mao F
Autoimmun Rev · 2025 Aug · PMID 40562293 · Publisher ↗
Inflammatory bowel disease (IBD) is a highly prevalent and recurrent autoimmune disorder characterized by dysregulation of the immune system leading to intestinal inflammation. Currently, available clinical treatments, s...
Inflammatory bowel disease (IBD) is a highly prevalent and recurrent autoimmune disorder characterized by dysregulation of the immune system leading to intestinal inflammation. Currently, available clinical treatments, such as mesalazine, are mainly used to alleviate symptoms but do not cure the disease. Mesenchymal stem cells (MSCs), as an emerging therapeutic tool, show potential in IBD through immunomodulatory effects, but their specific mechanisms need further exploration. Dendritic cells (DCs) are important antigen-presenting cells that play a key role in the immune response in IBD, although their specific mechanism of action remains largely uncovered. This review focuses on discussing MSCs and their derived exosomes in the modulation of DC in IBD, providing insight into the therapeutic potentials of MSCs in IBD.
Chimeric antigen receptor cell therapy: A revolutionary approach transforming cancer treatment to autoimmune disease therapy.
Wen R, Li B, Wu F … +12 more , Mao J, Azad T, Wang Y, Zhu J, Zhou X, Xie H, Qiu X, Hun M, Tian J, Zhang L, Hong K, Wen C
Autoimmun Rev · 2025 Aug · PMID 40562292 · Publisher ↗
Currently, autoimmune disorders are predominantly managed with broad-spectrum immunosuppressive agents and monoclonal antibodies, which can alleviate disease symptoms but are rarely curative and are frequently associated...
Currently, autoimmune disorders are predominantly managed with broad-spectrum immunosuppressive agents and monoclonal antibodies, which can alleviate disease symptoms but are rarely curative and are frequently associated with significant adverse effects. Autoreactive B cells play a key role in the pathogenesis of many autoimmune diseases; however, B-cell-depleting therapies such as rituximab have shown limited efficacy in certain autoimmune diseases, primarily due to the persistence of autoreactive B cells within lymphoid tissues and sites of inflammation. Consequently, there is an urgent need for more effective and targeted therapies for patients with severe and refractory autoimmune conditions. In this context, recent advancements in genetic engineering have facilitated the application of cell-based therapies, which have transitioned from oncology to treating autoimmune diseases. Therapies utilizing chimeric antigen receptor (CAR) engineered immune cells have emerged as a promising and potentially curative approach. Clinical trials targeting CD19-expressing B cells in B cell-driven autoimmune diseases, such as systemic lupus erythematosus (SLE), have yielded encouraging results, demonstrating durable remissions in otherwise treatment-resistant cases. In addition, novel strategies are being developed to broaden the therapeutic scope of CAR-based therapies in autoimmunity, including chimeric autoantibody receptor (CAAR)-T cells designed to eliminate autoantigen-specific B cells selectively and CAR-engineered regulatory T cells (CAR-Tregs) aimed at achieving antigen-specific immune modulation and restoration of self-tolerance. Despite these advances, several challenges persist, including short and long-term safety concerns, limited in vivo persistence, and the high costs associated with personalized cell manufacturing. Innovations in CAR design, such as logic-gated CARs, inducible suicide switches, and universal CAR constructs, are under active investigation to enhance safety, control, scalability, and clinical accessibility.
Impact and management of warm autoimmune haemolytic anaemia associated with systemic lupus erythematosus.
Pons-Estel GJ, Mosca M, Wallace DJ … +6 more , Zazzetti F, Leon A, Noël W, Pierce A, Ebrahim T, Murakhovskaya I
Autoimmun Rev · 2025 Aug · PMID 40562291 · Publisher ↗
Warm autoimmune haemolytic anaemia (wAIHA) is a rare autoantibody-mediated disorder that may occur in association with systemic lupus erythematosus (SLE). The clinical course of wAIHA is highly variable, ranging from ana...
Warm autoimmune haemolytic anaemia (wAIHA) is a rare autoantibody-mediated disorder that may occur in association with systemic lupus erythematosus (SLE). The clinical course of wAIHA is highly variable, ranging from anaemia compensated adequately by reticulocytosis to severe, life-threatening cases. While insights into the pathogenesis of wAIHA in SLE remain limited, emerging evidence highlights the risk factors and impact of wAIHA in the context of SLE. Management of wAIHA associated with SLE remains challenging as there is limited clinical evidence to support treatment decisions. New therapies, some that target underlying disease mechanisms relevant to both conditions, are in development. In this review, we examine the impact of wAIHA on clinical outcomes for patients with SLE, summarise the current management strategies along with unmet needs, and provide an update on novel therapeutic strategies.
Radio-labelled fibroblast activation protein inhibitors in interstitial lung diseases - a systematic review.
Bundgaard-Nielsen M, Johnsen RH, Mortensen J … +2 more , Shaker SB, Nielsen CTH
Autoimmun Rev · 2025 Aug · PMID 40544983 · Publisher ↗
BACKGROUND: Currently, no tools can monitor ongoing fibrotic activity properly, making early identification of and timely therapeutic intervention with antifibrotics in patients with progressive fibrosing interstitial lu...
BACKGROUND: Currently, no tools can monitor ongoing fibrotic activity properly, making early identification of and timely therapeutic intervention with antifibrotics in patients with progressive fibrosing interstitial lung disease (ILD) difficult. Fibroblast activation protein-α inhibitor (FAPI) radiotracers could address these challenges. OBJECTIVE: This review examines the association between pulmonary FAPI tracer uptake, fibrotic activity, and clinical parameters used for disease monitoring and prognostication in ILD to provide insights into its clinical potential. METHODS: In January 2025, a systematic literature search on PubMed, Ovid Medline, and Cochrane Library, utilizing the block-search strategy and snowballing, was conducted, and 13 studies were included. RESULTS: Both murine and human studies support that FAPI tracer uptake reflects fibrotic activity in ILDs, as uptake was consistently elevated in subject groups compared to controls. In murine ILD models, increased uptake was associated with fibrosis and fibroblast activation protein-α (FAP-α) expression upon histological examination. Uptake preceded the development of fibrosis on computed tomography (CT) and attenuated once fibrosis was established. In human ILD patients (Idiopathic pulmonary fibrosis (IPF) = 55, Connective tissue disease (CTD) ILD = 68, other ILDs = 55), FAPI uptake was localized to fibrotic lesions on high-resolution computed tomography (HRCT) and associated with increased FAP-α expression ex vivo. Uptake correlated with baseline pulmonary function tests (PFTs) and fibrosis extent on HRCT. Increased FAPI tracer uptake at baseline predicted disease progression upon follow-up. CONCLUSION: An increasing body of evidence supports that FAPI tracers hold great clinical potential for the management of ILD by accurately monitoring fibrotic disease activity and identifying patients at risk of progression. Further research is required to confirm these findings.
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