Autoimmunity Reviews[JOURNAL]
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200 papers
FcγRIIa in autoimmunity: Unraveling pathogenic mechanisms and therapeutic opportunities.
Zhu B, Cao X, Wang X … +5 more , Yu L, Zhou W, Zhu L, Yang Q, Rui K
Autoimmun Rev · 2026 Feb · PMID 41371427 · Publisher ↗
Autoantibodies, hallmark mediators of autoimmune diseases, drive pathogenesis through Fc receptors (FcRs) engagement. Among human FcRs, FcγRIIa is the most abundantly expressed subtype and plays a pivotal role in regulat...
Autoantibodies, hallmark mediators of autoimmune diseases, drive pathogenesis through Fc receptors (FcRs) engagement. Among human FcRs, FcγRIIa is the most abundantly expressed subtype and plays a pivotal role in regulating both innate and adaptive immune responses. Genetic polymorphisms and dysregulated FcγRIIa signaling are increasingly implicated in autoimmune pathogenesis. By governing immune cell activation, differentiation, and effector functions, FcγRIIa emerges as a central orchestrator of immune responses. Recent clinical studies have identified FcγRIIa as a promising therapeutic target in patients with autoimmune diseases, as well as in murine autoimmune models. This review outlines the structure and cellular expression profile of FcγRIIa and elucidates its role in immune regulation. Furthermore, we discuss its association with autoimmune pathogenesis and highlight FcγRIIa targeted therapeutics evaluated in past and ongoing clinical trials for autoimmune disease treatment.
Discrepancy between international guidelines and global laboratory practices in autoantibody testing for autoimmune hepatitis.
Bizzaro N, Bogdanos D
Autoimmun Rev · 2026 Feb · PMID 41360386 · Publisher ↗
Abstract loading — click title to view on PubMed.
Therapeutic approaches in adults with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): A review of current evidence.
Stögbauer J, Schegerer V, Klein C … +5 more , Pawlitzki M, Meuth SG, Aktas O, Groppa S, Fousse M
Autoimmun Rev · 2026 Feb · PMID 41344538 · Publisher ↗
Recent years have seen a considerable increase in knowledge pertaining to Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD). Nevertheless, a noteworthy degree of uncertainty remains within the neuro...
Recent years have seen a considerable increase in knowledge pertaining to Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD). Nevertheless, a noteworthy degree of uncertainty remains within the neurological community, primarily due to the often highly heterogeneous nature of the disease and the absence of approved long-term treatment options. In this article, we undertake a comprehensive review of the various treatment strategies and drug options available for the pharmacological treatment of acute attacks and relapses in MOGAD.
Targeting age-related cell-free DNA for prevention, early diagnosis and treatment of rheumatoid arthritis.
Ma N, Xu Y, Zhang D … +4 more , Zhang HT, Luo W, Cao Y, Wong VKW
Autoimmun Rev · 2026 Feb · PMID 41319827 · Publisher ↗
Cell-free DNA (cf-DNA) refers to extracellular DNA fragments released during cell death, which have been observed to accumulate with advancing age. Elevated cf-DNA concentrations have been detected in the plasma and dise...
Cell-free DNA (cf-DNA) refers to extracellular DNA fragments released during cell death, which have been observed to accumulate with advancing age. Elevated cf-DNA concentrations have been detected in the plasma and disease-affected tissues of patients with multiple disorders, particularly age-related autoimmune diseases such as rheumatoid arthritis (RA). Growing evidence supports the potential of cf-DNA as a biomarker for a broad spectrum of autoimmune and age-associated conditions, including cancer, systemic lupus erythematosus (SLE), and psoriasis. Fluctuations in cf-DNA levels and characteristics appear to be closely associated with disease onset, progression, severity, and prognosis. Importantly, emerging studies indicate that cf-DNA may not merely act as a passive biomarker but could also function as an active mediator contributing to RA pathogenesis through distinct immunological pathways. These insights suggest that cf-DNA represents a promising target for the development of innovative diagnostic, preventive, and therapeutic strategies. In this review, we summarize the current understanding of age-related cf-DNA in RA, highlight its potential immunopathological roles, and discuss recent advances in cf-DNA-based diagnostic tools, preventive approaches, and therapeutic interventions with possible clinical translational value.
Autoantibody internalization in myositis skeletal muscle: Emerging evidence, mechanistic insights, and therapeutic relevance.
Kirou RA, Pinal-Fernandez I, Mammen AL
Autoimmun Rev · 2026 Feb · PMID 41309016 · Full text
The inflammatory myopathies-including dermatomyositis, immune-mediated necrotizing myopathy, anti-synthetase syndrome, and overlap myositis-are systemic autoimmune diseases characterized by myositis-specific and myositis...
The inflammatory myopathies-including dermatomyositis, immune-mediated necrotizing myopathy, anti-synthetase syndrome, and overlap myositis-are systemic autoimmune diseases characterized by myositis-specific and myositis-associated autoantibodies targeting intracellular antigens. These diseases can be subclassified by autoantibody seropositivity, based on the understanding that each myositis autoantibody is associated with distinct clinical features. Traditionally, given the intracellular nature of their targets, myositis autoantibodies were thought to be non-pathogenic. However, this idea is now being challenged based on data from recent and older studies showing that autoantibodies reach their intracellular targets in vivo and exert functional pathogenic effects. In this review, we summarize experimental evidence supporting a model of pathogenic autoantibody internalization in the skeletal muscle of different inflammatory myopathies. We also address gaps in the evidence for this model, including the lack of a proven mechanism of autoantibody entry, while offering suggestions for future studies to fill these gaps. We discuss possible mechanisms of autoantibody entry, as well as the diagnostic, prognostic, and therapeutic implications of this model. Finally, we propose that autoantibodies targeting intracellular antigens in other autoimmune diseases-including certain autoimmune neurologic disorders, systemic sclerosis, systemic lupus erythematosus, and vasculitis-could potentially play a role in these conditions.
Extracellular vesicles in autoimmune diseases: Mechanistic underpinnings and precision medicine applications.
Mo W, Zhang Y, Zeng Y … +4 more , Zheng Y, Zhao S, Wang X, Fan X
Autoimmun Rev · 2026 Feb · PMID 41275948 · Publisher ↗
Autoimmune diseases constitute a collection of complex disorders characterized by abnormal immune responses directed against self-tissues. The pathogenesis of these diseases is strongly linked to the interaction of genet...
Autoimmune diseases constitute a collection of complex disorders characterized by abnormal immune responses directed against self-tissues. The pathogenesis of these diseases is strongly linked to the interaction of genetic predispositions and environmental influences. Clinically, autoimmune diseases present with heterogeneous manifestations, and their prevalence has been steadily rising, resulting in profound impacts on patients' physical and psychological health and creating a growing challenge for healthcare infrastructures. At present, nonspecific immunosuppressants are the main treatment method, but this method has limitations such as extensive immunosuppression and serious adverse reactions. Therefore, there is an urgent need to develop novel and targeted therapeutic strategies. As crucial mediators of intercellular communication, extracellular vesicles (EVs) have become significant actors in the control of inflammatory and immunological responses, showing great promise in both mechanistic studies and clinical applications. This study offers a comprehensive overview of current developments in EV research for the main autoimmune conditions, including inflammatory bowel disease, systemic lupus erythematosus, and rheumatoid arthritis. It further comprehensively discusses the potential clinical value of EVs from the perspectives of disease pathogenesis and biomarker development, aiming to offer theoretical support and innovative directions for the clinical application of EV-based diagnostics and treatments, as well as for the realization of precision medicine in autoimmune disorders.
Sporadic late-onset nemaline myopathy (SLONM): Data from a case series and literature review of 144 patients.
Lauletta A, Forcina F, Merlonghi G … +10 more , Fionda L, Leonardi L, Costanzo R, Tufano L, Rossini E, Marando D, Vera V, Antonini G, Morino S, Garibaldi M
Autoimmun Rev · 2026 Feb · PMID 41270914 · Publisher ↗
Sporadic Late-Onset Nemaline Myopathy (SLONM) is an acquired myopathy presenting in adulthood with progressive proximal and axial muscle weakness. A substantial proportion of cases are associated with monoclonal gammopat...
Sporadic Late-Onset Nemaline Myopathy (SLONM) is an acquired myopathy presenting in adulthood with progressive proximal and axial muscle weakness. A substantial proportion of cases are associated with monoclonal gammopathy of undetermined significance (MGUS), referred to as SLONM-MGUS, suggesting a potential immune-mediated pathogenesis. Although the presence of MGUS has clinical and therapeutic implications, its exact role in disease severity and progression remains unclear. We aimed to characterize clinical, pathological, and prognostic differences between SLONM-MGUS and SLONM without MGUS (SLONM-noMGUS). We conducted a systematic review of SLONM case series published over the past 25 years, supplemented by a single-center case series of five additional patients from our institution (Sant'Andrea Hospital, Rome). Eligible subjects included adult patients diagnosed with SLONM based on clinical features and muscle biopsy demonstrating nemaline rods. Data on demographics, laboratory parameters, histopathological findings, treatments and outcomes were extracted and compared between SLONM-MGUS and SLONM-noMGUS cohorts. Of the 144 patients analyzed, 47 % were classified as SLONM-MGUS. These patients exhibited more severe clinical manifestations, including increased respiratory involvement (p = 0.006). Histopathologically, SLONM-MGUS revealed more prominent nemaline rods (p = 0.032), often accompanied by cytoplasmic bodies and lobulated fibers, and frequently required repeat muscle biopsies for diagnosis (p = 0.0285). Inflammatory infiltrates were less frequent in SLONM-MGUS (p = 0.0176). Functional outcomes were significantly worse in this group, with reduced likelihood of full recovery (p = 0.013) and higher rates of non-ambulatory status (p = 0.01). Patients receiving dual or more treatment regimens, particularly those including IVIg and/or autologous stem cell transplantation (ASCT), had more favorable outcomes. These findings indicate that SLONM-MGUS represents a more severe phenotype of SLONM with distinct clinico-pathological features and poorer prognosis. Notably, combined treatment regimens, including IVIg and/or ASCT, were associated with improved outcomes, highlighting the importance of early recognition and aggressive therapeutic strategies in selected patients.
Regulated cell death in systemic lupus erythematosus: Key pathways and targeted therapies.
Deng S, Hu Z, Cai S … +1 more , Dong L
Autoimmun Rev · 2026 Jan · PMID 41265736 · Publisher ↗
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by pathological auto-antibody production and severe immune dysregulation. Dysfunction in regulated cell death (RCD) pathways is crucial in...
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by pathological auto-antibody production and severe immune dysregulation. Dysfunction in regulated cell death (RCD) pathways is crucial in SLE development. Abnormal cell death and cell debris clearance disorder within tissues promote the exposure and accumulation of auto-antigens, activate self-reaction B cells, and amplify interferon type I (IFN-I) reaction. Meanwhile, immune microenvironment disorder caused by abnormal RCD of immune cells exacerbate this response. The review systematically expounds the pathogenic mechanisms of both classical and novel RCD pathways in SLE. By comparing shared and disease-specific RCD dysregulation between SLE and other autoimmune diseases, we evaluate innovative RCD-targeted therapies, offering new insights on SLE pathogenesis and precision treatment.
Senescent CD4 T cells and autoimmune diseases: mechanisms and therapeutic prospects.
Hu Y, He L, Long H
Autoimmun Rev · 2026 Jan · PMID 41248726 · Publisher ↗
Senescent CD4⁺ T cells exhibit classical features of T-cell senescence-including telomere attrition, reduced proliferative capacity, and an upregulated senescence-associated secretory phenotype (SASP)-while also displayi...
Senescent CD4⁺ T cells exhibit classical features of T-cell senescence-including telomere attrition, reduced proliferative capacity, and an upregulated senescence-associated secretory phenotype (SASP)-while also displaying unique characteristics. Notably, they maintain relatively healthy mitochondrial mass compared with senescent CD8⁺ T cells, a distinction that influences their roles in immune regulation and tissue pathology. Multiple signaling pathways, such as the ATM-DDR-p53 axis, AMPK-TAB1-p38 cascade, mTOR signaling, mitochondrial-ROS axis, and IL-7/IL-2 cytokine networks, are dysregulated during the senescence of CD4⁺ T cells. Importantly, senescent CD4⁺ T cells can promote chronic inflammation, disrupt immune homeostasis, and remodel tissue microenvironments through the secretion of SASP components (e.g., IL-6, IL-8, TNF-α, and MMPs). They also have the potential to enhance antibody secretion by B cells, ultimately contributing to tissue-specific damage. These aberrant cells have been shown to accumulate in several autoimmune diseases (ADs), including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and systemic sclerosis (SSc). Targeting senescent CD4⁺ T cells with senotherapeutic agents and SASP inhibitors has been shown to markedly suppress AD progression, underscoring the translational potential of this therapeutic approach. However, more specific senescence markers are needed to accurately identify senescent CD4⁺ T cells. This review synthesizes current knowledge on senescent CD4⁺ T cells and their involvement in autoimmune diseases. Future research should prioritize elucidating their pathogenic mechanisms and developing targeted therapeutic strategies to mitigate their detrimental effects in ADs.
Drug- and vaccine induced ANCA-associated vasculitis: An overview.
Cohen Tervaert JW
Autoimmun Rev · 2026 Jan · PMID 41213309 · Publisher ↗
Many different drugs and/or vaccines may cause vasculitis which can be sometimes very severe. The clinical presentation varies from isolated skin vasculitis to multi-organ involvement with pulmonary-renal manifestations...
Many different drugs and/or vaccines may cause vasculitis which can be sometimes very severe. The clinical presentation varies from isolated skin vasculitis to multi-organ involvement with pulmonary-renal manifestations and/or cerebral vasculitis. Whereas causality is difficult to prove and rechallenges are considered unethical, pathophysiological mechanisms suggesting causality have been demonstrated for drugs such as hydralazine, propylthiouracil, levamisole, and immune checkpoint inhibitors. An important pathophysiological mechanism of drug-induced anti-neutrophil autoantibody (ANCA)-associated vasculitis is the fact that several drugs have been demonstrated to increase the formation of neutrophil extracellular traps which may result in the development of autoimmunity. The first step in medical management of drug-induced ANCA-associated vasculitis is discontinuation of the offending drug and a transparent discussion with the patient regarding the possibility that the drug or the vaccine may have caused vasculitis. Additional treatment with steroids and immunosuppressants is often needed in more severe cases of ANCA-associated vasculitis. In general, however, the long-term prognosis of drug-induced ANCA-associated vasculitis is more favorable compared to the prognosis of idiopathic ANCA-associated vasculitis. Physicians that are treating patients with vasculitis should be aware of the possible role of drugs and vaccines in the development ANCA-associated vasculitis.
Ferritinophagy in inflammatory and autoimmune diseases: Mechanistic insights and therapeutic potentials.
Wang Y, Li Y, Jiang J … +3 more , Hong Y, Gao S, Hua C
Autoimmun Rev · 2026 Jan · PMID 41176258 · Publisher ↗
Ferritinophagy, a selective form of autophagy mediated by nuclear receptor coactivator 4 (NCOA4), degrades ferritin to regulate intracellular iron homeostasis and has emerged as an important process in inflammatory and a...
Ferritinophagy, a selective form of autophagy mediated by nuclear receptor coactivator 4 (NCOA4), degrades ferritin to regulate intracellular iron homeostasis and has emerged as an important process in inflammatory and autoimmune diseases. By controlling ferritin turnover, ferritinophagy affects labile iron levels and ferroptosis, an iron-dependent cell death driven by lipid peroxidation, and interacts with multiple immune regulatory pathways. This process is modulated by signaling networks such as MAPK, cGAS-STING, NF-κB, AMPK/mTOR, and NRF2, which link iron metabolism to inflammatory responses. Aberrant ferritinophagy has been implicated in conditions including sepsis, osteoarthritis, asthma, rheumatoid arthritis, and systemic lupus erythematosus. Preclinical studies demonstrate that strategies such as inhibiting the JNK-JUN or cGAS-STING pathways, or applying iron chelators like deferoxamine, can reduce iron overload, limit ferroptosis, and attenuate inflammation. Despite these advances, further work is needed to delineate disease-specific regulatory mechanisms and to translate ferritinophagy modulation into safe and effective therapies. This review summarizes current mechanistic insights and therapeutic prospects, highlighting ferritinophagy as a promising target for managing inflammatory and autoimmune disorders.
Are the 2023 ACR/EULAR classification criteria a step forward in the management of antiphospholipid syndrome? A literature-based and clinical practice appraisal.
Alijotas-Reig J, Marques-Soares J, Esteve-Valverde E … +7 more , Anunciación-Llunell A, Andrada C, Ockova M, Hoxha A, Khamashta MA, Shoenfeld Y, Miró-Mur F
Autoimmun Rev · 2026 Jan · PMID 41173354 · Publisher ↗
Antiphospholipid syndrome (APS) is an autoimmune disease (AID) without defined diagnostic criteria, but having classification criteria, as happens in most AID. Until 2023, we were using 2006 Sydney classification criteri...
Antiphospholipid syndrome (APS) is an autoimmune disease (AID) without defined diagnostic criteria, but having classification criteria, as happens in most AID. Until 2023, we were using 2006 Sydney classification criteria. Although they had a research purposes, in the real life they have been used as a diagnostic tool, equating classification with diagnostic. From July 2023, these criteria were revisited by American College of Rheumatology and European League Against Rheumatism (ACR/EULAR) panel of experts. This recently reported set of classification criteria underlie that only should be used for research purposes. They prioritises specificity ̵ 99 % ̵ at the cost of sensitivity ̵ 84 % ̵ ACR/EULAR criteria consider 6 clinical and 2 laboratory domains. Although new clinical items have been included, improving overall the inclusion of patients and, indirectly diagnosis, i.e., thrombocytopenia, cardiac valvular involvement and microvascular thrombosis, a remarkable number of patients with putative aPL-related disorders could leave out of classification as having APS, and in the real life, losing the opportunity to manage them appropriately. Consequently, these patients will be prone to suffer new events, thrombotic or obstetric, as have been already demonstrated. This manuscript focuses on the pros and cons of the clinical and laboratory domains of these new criteria and their impact not only on the clinical point of view, but also in the APS research field. Using 6 clinical cases, we provide readers with a sense of diagnostic certainties and uncertainties, and their shortcomings in the context of the ACR/EULAR APS classification.
Environmental toxins and toxic metals in autoimmune diseases: Sex differences, hormonal influences, and immune dysregulation.
Bjørklund G, Wallace DR, Kangarlou K … +2 more , Hossain F, Peana M
Autoimmun Rev · 2026 Jan · PMID 41173353 · Publisher ↗
Environmental toxins, including toxic metal(oid)s such as mercury, lead, cadmium, and arsenic, as well as endocrine-disrupting chemicals like bisphenol A and phthalates, play a critical role in the onset and progression...
Environmental toxins, including toxic metal(oid)s such as mercury, lead, cadmium, and arsenic, as well as endocrine-disrupting chemicals like bisphenol A and phthalates, play a critical role in the onset and progression of autoimmune diseases. These substances accumulate in biological tissues and disrupt immune homeostasis through oxidative stress, molecular mimicry, and epigenetic modifications, mechanisms that contribute to autoantibody production and chronic inflammation, hallmarks of autoimmunity. Women are disproportionately affected by autoimmune diseases due to inherent differences in immune function, hormonal regulation, and genetic susceptibility. Estrogen, a key immunomodulatory hormone, can amplify immune responses and promote autoantibody generation. Its interaction with environmental toxins further exacerbates immune dysregulation, increasing female vulnerability to conditions such as systemic lupus erythematosus, rheumatoid arthritis, and autoimmune thyroid disorders. Hormonal fluctuations during puberty, pregnancy, and menopause additionally influence toxin metabolism and detoxification efficiency, compounding the risk of immune imbalance and disease onset in women. This review synthesizes current evidence on the mechanisms through which environmental toxicants contribute to autoimmune pathogenesis, with particular focus on sex-specific vulnerabilities. It explores the role of hormonal-immune-environment interactions across the female lifespan and highlights emerging research on epigenetic inheritance, gut dysbiosis, and biomarker development. By integrating mechanistic, epidemiological, and clinical findings, this review aims to inform targeted strategies for prevention, early detection, and risk reduction of environmentally driven autoimmune diseases.
Extending the discussion: Cannabis based therapies in inflammatory bowel disease a letter to the editor.
Yaratha L, Deogaonkar A, Borum ML
Autoimmun Rev · 2026 Jan · PMID 41167372 · Publisher ↗
Abstract loading — click title to view on PubMed.
IL-33 in Spondyloarthritis, the missing key.
Verhoeven F, Hannani D, Demougeot C … +4 more , Meyer F, Wendling D, Prati C, Baillet A
Autoimmun Rev · 2026 Jan · PMID 41135784 · Publisher ↗
Interleukin-33 (IL-33), an alarmin released upon tissue stress or damage, has gained increasing interest in the pathophysiology of inflammatory diseases such as spondyloarthritis (SpA). Acting through its receptor ST2, I...
Interleukin-33 (IL-33), an alarmin released upon tissue stress or damage, has gained increasing interest in the pathophysiology of inflammatory diseases such as spondyloarthritis (SpA). Acting through its receptor ST2, IL-33 contributes to the activation of type 2 innate lymphoid cells, Th17 responses, and macrophage polarization. It is involved in key musculoskeletal features of SpA, including enthesitis, synovitis, and axial inflammation, and may also play a role in associated extra-articular manifestations such as gut, skin, eyes inflammation. Preclinical studies targeting the IL-33/ST2 axis have shown promising results, with a reduction of arthritis severity, structural joint damage, and inflammation. The dual role of IL-33 in inflammation and bone metabolism further supports its relevance in SpA. Depending on the cellular context, IL-33 can inhibit osteoclast differentiation or promote pathological bone formation, particularly through the induction of pro-osteogenic macrophages. These findings open the possibility of targeting IL-33 not only to control inflammation but also to modulate structural outcomes, including new bone formation. As current biologics such as anti-TNFα or anti-IL-17 therapies do not fully prevent structural progression in all patients, IL-33 represents an attractive complementary target. This review discusses the emerging role of the IL-33/ST2 pathway in SpA and its potential therapeutic implications.
VE/VCO at ventilatory threshold and peak VO in CPET studies of patients with scleroderma-associated PAH: A systematic review and meta-analyses.
Better J, Leroy S, Ninaber MK … +8 more , Trakada G, Kesikburun B, Rosenkranz S, Ewert R, Habedank D, Dumitrescu D, Kouchit Y, Martis N
Autoimmun Rev · 2026 Jan · PMID 41130314 · Publisher ↗
CONTEXT: Pulmonary arterial hypertension (PAH) is one of the leading causes of mortality in patients with systemic sclerosis (SSc). Cardiopulmonary exercise testing (CPET) has been studied to detect SSc-associated PAH. O...
CONTEXT: Pulmonary arterial hypertension (PAH) is one of the leading causes of mortality in patients with systemic sclerosis (SSc). Cardiopulmonary exercise testing (CPET) has been studied to detect SSc-associated PAH. OBJECTIVES: To evaluate the diagnostic value of the ventilatory equivalent for CO at anaerobic or ventilatory threshold [VE/VCO(VeT)] and peak oxygen uptake (peak VO) for SSc-associated PAH obtained by CPET. METHODS: A systematic database search from 1993 to 2024 and meta-analyses were performed according to PRISMA guidelines to include original studies relating to SSc and CPET reporting VE/VCO(VeT) and peak VO. The random-effects model was chosen for the meta-analyses studying VE/VCO(VeT), indexed and predicted percentage (%pred.) peak VO, respectively. Meta-regression was only performed for VE/VCO(VeT) with covariates defined as the percentage of limited cutaneous disease, percentage of interstitial lung disease, and %pred. of peak VO. RESULTS: Out of 206 studies, 941 SSc patients from 15 studies were included. VE/VCO(VeT) (11 studies, n = 850) was statistically lower in patients without PAH (32.68 ± 5.42 vs. 39.81 ± 9.32) with a mean effect size of -1.182 (95 %CI, -1.691 to -0.672; p < 0.001) (I = 86 %). The mean effect size for weight-indexed peak VO (11 studies, n = 848) was 0.713 (95 %CI, 0.371 to 1.054; p < 0.001) with higher values in patients without PAH (16.47 ± 4.62 vs. 13.61 ± 4.16 mL/kg/mn) (I = 70 %). Similarly, the mean effect size for %pred. Peak VO (12 studies, n = 850) was 0.659 (95 %CI, 0.425 to 0.894; p < 0.001) reflecting higher values in patients without PAH (74.00 ± 17.50 vs. 54.84 ± 18.14 %pred.) (I = 37 %). Meta-regression analysis of data from 7 studies did not yield significant p values for the covariates. CONCLUSIONS: The effect size of each meta-analysis indicates that higher VE/VCO(VeT) and lower peak VO may be considered as independent CPET markers of PAH in patients with SSc. CPET is a non-invasive and safe procedure for exploring dyspnoea in patients with SSc and, in association with conventional imaging techniques, may provide a reliable assessment of the presence of PAH.
Immune checkpoint inhibitor-induced inflammatory arthritis vs rheumatoid arthritis: A comparative review.
Georgios I, Fani S, Dmitrios B … +2 more , David L, Dimitrios D
Autoimmun Rev · 2026 Jan · PMID 41115565 · Publisher ↗
Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are frequently accompanied by immune-related adverse events (irAEs). Among these, ICI-induced inflammatory arthritis (ICI-IA)...
Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are frequently accompanied by immune-related adverse events (irAEs). Among these, ICI-induced inflammatory arthritis (ICI-IA) has emerged as the most common musculoskeletal toxicity, often mimicking rheumatoid arthritis (RA) in its clinical and imaging features. This narrative review synthesizes current evidence comparing ICI-IA with RA across epidemiology, pathophysiology, clinical presentation, imaging, treatment, and prognosis. While both entities share overlapping manifestations such as polyarthritis, synovitis, and joint erosions, ICI-IA is typically seronegative, arises subacutely after ICI initiation, and exhibits distinct immunopathologic signatures, including cytotoxic CD8+ T-cell predominance and unique B-cell alterations. ICI-IA may persist after ICI cessation, with chronic disease linked to improved oncologic outcomes. Therapeutic strategies require balancing arthritis control and preservation of anti-tumor immunity. Glucocorticoids and conventional disease modifying anti-rheumatic drugs (cDMARDs) are key players with proven safety and efficacy, whereas biologic therapies remain reserved for severe or refractory cases mainly due to cancer progression concerns. Furthermore, early rheumatology referral improves patient outcomes and reduces glucocorticoid exposure. Understanding the differences between ICI-IA and RA is essential for optimizing diagnosis, guiding individualized approach and applying precision medicine at the crossroads of oncology and rheumatology.
Sex-specific mechanisms in the pathogenesis and progression of chronic kidney disease.
Li G, Xu Z, Yang H … +7 more , Zhang D, Liu B, Song Y, Li Q, Zhang Y, Zhou H, Wang Y
Autoimmun Rev · 2026 Jan · PMID 41106576 · Publisher ↗
Chronic kidney disease (CKD) is a growing global public health concern, marked by increasing prevalence and substantial economic burden. Notably, CKD demonstrates significant physiological sex differences. Epidemiologica...
Chronic kidney disease (CKD) is a growing global public health concern, marked by increasing prevalence and substantial economic burden. Notably, CKD demonstrates significant physiological sex differences. Epidemiological evidence indicates that men are more susceptible to developing CKD in early to middle adulthood due to accelerated declines in renal function, whereas postmenopausal women exhibit a sharp rise in CKD incidence and progression. These findings suggest that sex hormones may play a critical regulatory role in CKD pathogenesis. The "bidirectional effects" of sex hormones are considered a fundamental mechanism driving these sex-based disparities. Androgens exacerbate renal inflammation and fibrosis by activating the TGF-β/TNF-α axis and the renin-angiotensin-aldosterone system (RAAS)/20-HETE pathway, in concert with NLRP3 inflammasome activation, thereby worsening glomerular hypertension and metabolic dysfunction. In contrast, estrogens exert protective effects by inhibiting RAAS activity, upregulating the ACE2/Ang-(1-7) pathway, activating the GPER/Sirt1 signaling network, and enhancing antioxidant capacity, thereby preserving renal hemodynamic homeostasis. Furthermore, this review incorporates a range of additional factors-including hormone-like compounds, sex-specific gut microbiota-host metabolic interactions, sex chromosome inactivation or loss, ectopic lipid deposition, and unfavorable lifestyle behaviors-to construct a comprehensive pathological model of sex-specific CKD progression. Elucidating the mechanisms by which sex differences influence kidney disease, and identifying sex-dependent contributors to CKD onset and advancement, may provide critical insights for developing personalized therapeutic strategies.
Association between weather conditions and rheumatoid arthritis: A systematic review and meta-analysis.
Hu C, Wu J, Luo Y … +4 more , Zhu Y, Chang R, Qian S, Ding X
Autoimmun Rev · 2026 Jan · PMID 41083015 · Publisher ↗
OBJECTIVES: Weather conditions have been suggested to influence the clinical manifestations of rheumatoid arthritis (RA), but current evidence remains inconsistent. This meta-analysis aimed to evaluate the association be...
OBJECTIVES: Weather conditions have been suggested to influence the clinical manifestations of rheumatoid arthritis (RA), but current evidence remains inconsistent. This meta-analysis aimed to evaluate the association between meteorological factors and RA disease activity. METHODS: PubMed, Web of Science, EMBASE, and the Cochrane Library were searched from inception to March 25, 2025. Two reviewers independently screened and extracted data according to predefined criteria. A random-effects model was used to pool results. Meta-regression analyses were performed to explore potential sources of heterogeneity across studies. Publication bias was assessed using Egger's test, Begg's test, and funnel plots. Sensitivity analyses were conducted using a leave-one-out approach to examine the impact of each individual study on the pooled estimates. RESULTS: A total of 16,503 records were identified through the literature search, of which eight studies met the inclusion criteria and were included in the meta-analysis. The pooled results indicated no significant overall association between temperature, atmospheric pressure, humidity, or wind speed and RA pain. In addition, temperature was negatively correlated with TJC (pooled Fisher's Z = -0.08, 95 % CI -0.151 to -0.009, P = 0.028 < 0.05, summary r = -0.080, 95 % CI -0.150 to -0.009), and atmospheric pressure was negatively correlated with SJC (pooled Fisher's Z = -0.075, 95 % CI -0.115 to -0.036, P < 0.001, summary r = -0.075, 95 % CI -0.114 to -0.036), both with low heterogeneity. No other significant associations were observed. CONCLUSIONS: Specific meteorological factors, temperature and atmospheric pressure, may modestly affect RA symptoms. These findings may contribute to individualized disease management and guide future research on environmental influences in autoimmune diseases.
MTHFR polymorphisms in autoimmune diseases: Mechanistic and clinical perspectives.
Sun T, Wu Y, Kong L … +5 more , Wang J, Zhang F, Liu Y, Gao J, Liu Y
Autoimmun Rev · 2026 Jan · PMID 41083014 · Publisher ↗
The methylenetetrahydrofolate reductase (MTHFR) gene encodes a crucial enzyme in folate metabolism, serving as a central regulator of homocysteine homeostasis and one‑carbon metabolic pathways. This review synthesizes cu...
The methylenetetrahydrofolate reductase (MTHFR) gene encodes a crucial enzyme in folate metabolism, serving as a central regulator of homocysteine homeostasis and one‑carbon metabolic pathways. This review synthesizes current evidence on the mechanistic and clinical implications of two common MTHFR polymorphisms, C677T and A1298C, in autoimmune pathogenesis. We critically examine their contributions to inflammatory responses, endothelial dysfunction, immune imbalance, and epigenetic modifications. Furthermore, we analyze population-specific associations between these variants and susceptibility to eight autoimmune disorders, genotype-phenotype correlations related to clinical manifestations and comorbidities, as well as pharmacogenomic interactions influencing response to methotrexate therapy. By integrating genetic, molecular, and clinical insights, this review highlights the translational potential of MTHFR genotyping for improving risk stratification and personalized treatment strategies in autoimmune and immune-mediated inflammatory conditions.
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