Autoimmunity Reviews[JOURNAL]
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200 papers
Cognitive impairment in systemic autoimmune and inflammatory diseases: A narrative review focused on ANCA-associated vasculitis, sarcoidosis, Sjögren's syndrome, systemic sclerosis, and Behçet's disease.
Camard M, Urbain F, Noel N
Autoimmun Rev · 2025 Nov · PMID 40769406 · Publisher ↗
Cognitive impairment is an increasingly recognized feature of systemic autoimmune and inflammatory diseases, yet remains underdiagnosed and insufficiently studied beyond systemic lupus erythematosus. In this narrative re...
Cognitive impairment is an increasingly recognized feature of systemic autoimmune and inflammatory diseases, yet remains underdiagnosed and insufficiently studied beyond systemic lupus erythematosus. In this narrative review, we explore the prevalence, clinical profiles, and pathophysiological mechanisms of cognitive dysfunction in five systemic diseases: ANCA-associated vasculitis (AAV), primary Sjögren's syndrome (pSS), systemic sclerosis (SSc), sarcoidosis, and Behçet's disease (BD). We conducted a structured literature search in PubMed and Embase to identify relevant studies published between 1954 and 2024. Reported prevalence varies widely: ∼30 % in AAV, 0-35 % in sarcoidosis, 10-80 % in pSS, 8-65 % in SSc, and 30-100 % in BD. Executive dysfunction and attention deficits predominate. In some cases-particularly in AAV and BD-cognitive decline may reflect direct central nervous system involvement, but many patients report cognitive complaints without overt neurological manifestations or imaging abnormalities. Proposed mechanisms include blood-brain barrier disruption, cytokine-driven neuroinflammation (notably IL-6, TNF-α, IFN-γ, BAFF), autoantibody-mediated synaptic toxicity, and cerebral hypoperfusion linked to small-vessel vasculopathy. Glial activation and neuroimmune dysregulation are recurring findings in animal models and functional imaging studies. White matter lesions and abnormal brain perfusion on MRI or SPECT are frequently observed in asymptomatic patients. Comorbid symptoms such as depression, fatigue, pain, and small fiber neuropathy may exacerbate or mimic cognitive dysfunction. Despite its prevalence and impact on quality of life, cognitive dysfunction is rarely screened, partly due to a lack of standardized tools. Harmonized neurocognitive assessment protocols and longitudinal studies are urgently needed to improve understanding, detection, and management of cognitive impairment, and support its integration into routine care.
Unmet needs and emerging pharmacotherapies for autoimmune connective tissue disease-associated interstitial lung diseases.
Kondoh Y, Fujii T, Inoue Y … +1 more , Atsumi T
Autoimmun Rev · 2025 Nov · PMID 40769405 · Publisher ↗
Autoimmune connective tissue disease associated with interstitial lung disease (CTD-ILD) includes rheumatoid arthritis-associated ILD, systemic sclerosis-associated-ILD, and several other ILDs. Many patients with CTD-ILD...
Autoimmune connective tissue disease associated with interstitial lung disease (CTD-ILD) includes rheumatoid arthritis-associated ILD, systemic sclerosis-associated-ILD, and several other ILDs. Many patients with CTD-ILD-as well as individuals with other ILDs-develop a progressive pulmonary fibrosis (PPF) similar to idiopathic pulmonary fibrosis (IPF). PPF is characterized by worsening respiratory symptoms, declining lung function despite current pharmacotherapies, and ultimately early death. Current pharmacotherapies for CTD-ILD and PPF include glucocorticoids, immunosuppressants, and anti-fibrotic agents. Due to the scarcity of randomized clinical trials for CTD-ILD, many pharmacotherapies are generally administered off-label (although several are approved in Japan), with notable exceptions including nintedanib, an anti-fibrotic agent approved for SSc-ILD and chronic progressive fibrosing ILD in several countries. As the available agents only slow the decline of pulmonary function and are associated with treatment-limiting side effects, there is a need for more efficacious and tolerable pharmacotherapies for CTD-ILD and PPF. Promising compounds in clinical trials include nerandomilast (a preferential phosphodiesterase 4B inhibitor), admilparant (a lysophosphatidic acid receptor 1 antagonist), and inhaled treprostinil (a prostacyclin analogue). Nerandomilast may have both anti-fibrotic and immunomodulatory properties; in preclinical models of PPF, it reduced neutrophils and macrophages and down-regulated pro-fibrotic signaling pathways. Hopefully, therefore, this pipeline will produce new medications to ease the collectively large burden of CTD-ILD and PPF.
Systemic auto-inflammatory diseases, auto-immune diseases and immune deficiencies: From independent to overlapped diseases approach.
Parentelli AS, Lopes AA, Rieux-Laucat F … +1 more , Hermine O
Autoimmun Rev · 2025 Nov · PMID 40769404 · Publisher ↗
Systemic AutoInflammatory Diseases (SAIDs), AutoImmune Diseases (AIDs), and Primary Immune Deficiencies (PIDs) were formely considered independent, even opposing, conditions. SAIDs were associated with the innate immune...
Systemic AutoInflammatory Diseases (SAIDs), AutoImmune Diseases (AIDs), and Primary Immune Deficiencies (PIDs) were formely considered independent, even opposing, conditions. SAIDs were associated with the innate immune system, involving dysregulation of inflammation and recurrent episodes of systemic inflammation without an infectious process. Their original definition did not involve autoreactive cells or autoantibodies. In contrast, PIDs were characterised by defects in the adaptive or innate immune system, leading to recurrent infections and immune dysfunction. AIDs were inflammatory diseases also characterised by dysregulation of the immune system attacking its own tissues through autoreactive cells or autoantibodies. Nevertheless, advancements in genetics and a deeper understanding of T-cell development and signalling, immune tolerance, the complement pathway and inflammation have revealed that these conditions are overlapping diseases with shared immune system dysfunctions. These diseases now represent a continuum within a broader spectrum of disorders known as "Inborn Errors of Immunity". However, this term is not suitable as it does not fully encompass cases arising from somatic mutations and can be stigmatising for patients. Therefore, we propose the terms "Primary Immune Deficiencies and Dysregulations" (PIDDs) or simply "Primary Immune Disorders" (PIDs) as more appropriate alternatives. Thus, this article aims to describe known diseases where autoimmunity, autoinflammation and primary immunodeficiencies overlap, along with some mechanisms that may explain these interconnections. To our knowledge, no comprehensive reviews on this topic currently exist, despite its significance in modifying our understanding of these diseases, their treatment, and associated research.
Removal notice to "Relapsing polychondritis: A clinical update" [Autoimmunity Reviews 15_6 (2016) 539-543].
Longo L, Greco A, Rea A … +3 more , Vasco VRL, De Virgilio A, De Vincentiis M
Autoimmun Rev · 2025 Aug · PMID 40759075 · Publisher ↗
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Points to consider in the management of ANCA-associated vasculitis.
Papadopoulou M, Karamanakos A
Autoimmun Rev · 2025 Nov · PMID 40754136 · Publisher ↗
Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is characterized by inflammation and necrosis of small to medium blood vessels that frequently present with organ- or life-threatening manifestations...
Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is characterized by inflammation and necrosis of small to medium blood vessels that frequently present with organ- or life-threatening manifestations. Although significant therapeutic advances have improved outcomes, many areas in the management of AAV remain controversial or insufficiently defined. Key areas of debate include the choice of induction therapy-particularly the potential benefits of combining rituximab and cyclophosphamide-and the role of adjunctive therapies such as avacopan and plasma exchange. Additional challenges involve determining the optimal duration and dosing of maintenance therapy, strategies for relapse prediction and prevention, appropriate glucocorticoid tapering, the use of fixed versus biomarker-guided maintenance regimens, and the potential for withholding maintenance therapy in select patient populations. Despite multiple high-quality randomized controlled trials and international guidelines, clinical practice remains heterogeneous. The emergence of novel therapies is promising in helping to address these gaps and may provide effective treatment options for patients with resistant or refractory disease. This review summarizes current controversies and challenges in the treatment of AAV and provides a practical, evidence-based framework to support clinical decision-making.
Neutrophil extracellular traps and neuropsychiatric lupus: Signaling pathways involved in NET formation and mechanisms affecting the central nervous system.
Guan X, He X, Liu L
Autoimmun Rev · 2025 Nov · PMID 40752542 · Publisher ↗
Neuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication of systemic lupus erythematosus (SLE) that affects the central or peripheral nervous system. The clinical management of NPSLE faces significa...
Neuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication of systemic lupus erythematosus (SLE) that affects the central or peripheral nervous system. The clinical management of NPSLE faces significant challenges due to the absence of specific diagnostic biomarkers and the lack of standardized, evidence-based diagnostic and therapeutic protocols. Therefore, a comprehensive understanding of the pathogenesis of NPSLE and the exploration of novel therapeutic targets have become urgent priorities in current research. Recent studies have demonstrated that neutrophils and their hallmark product, neutrophil extracellular traps (NETs), play a central role in various pathological processes of NPSLE, with blood-brain barrier (BBB) disruption and the subsequent inflammatory cascade being particularly critical. This paper provides a systematic review of the molecular regulatory network of neutrophils in NPSLE, focusing on the mechanisms by which neutrophils mediate neuroimmune microenvironmental disorders through BBB damage, with the goal of offering a theoretical foundation for the precise diagnosis and treatment of this disease.
STING-inflammasome axis in autoimmune diseases and inflammation-related disease.
Chai S, Xu H, Liu R … +1 more , Cai C
Autoimmun Rev · 2025 Nov · PMID 40752541 · Publisher ↗
The STING-inflammasome axis predominantly functions to transmit signals generated from cGAS-STING-mediated cytosolic DNA recognition, thereby inducing and potentiating inflammasome activation and amplifying immune respon...
The STING-inflammasome axis predominantly functions to transmit signals generated from cGAS-STING-mediated cytosolic DNA recognition, thereby inducing and potentiating inflammasome activation and amplifying immune responses. However, under specific circumstances, the inflammasome can reciprocally modulate STING activity. This dynamic relationship comprises a canonical upstream-downstream activation cascade complemented by bidirectional interactions and feedback loops within the intricate immune regulatory network. Accumulating evidence underscores the pivotal involvement of the STING-inflammasome axis in diverse host defense mechanisms and inflammatory disorders, including autoimmune diseases, sterile inflammatory conditions, carcinogenesis, and neurodegenerative diseases. In this comprehensive review, we systematically summarize the current understanding of the contributions and underlying mechanisms of the STING-inflammasome axis in physiological and pathological processes. Additionally, we conduct an in-depth exploration of the translational potential of targeting this axis for preventive and therapeutic interventions, offering novel insights into future research directions and clinical applications.
Specialized pro-resolving mediators and autoimmunity: Recent insights and future perspectives.
Vomero M, Lamberti L, Corberi E … +8 more , Currado D, Marino A, Berardicurti O, Fava M, Leuti A, Maccarrone M, Giacomelli R, Navarini L
Autoimmun Rev · 2025 Nov · PMID 40744143 · Publisher ↗
Inflammation is a response to injuries involving multiple cellular and molecular mechanisms. Different stimuli, such as trauma or microbial invasion, trigger an acute inflammatory response consisting, at least in princip...
Inflammation is a response to injuries involving multiple cellular and molecular mechanisms. Different stimuli, such as trauma or microbial invasion, trigger an acute inflammatory response consisting, at least in principle, of two phases: initiation and resolution. Although the acute phase of inflammatory response represents a protective and usually self-limited mechanism, it can sometimes persist and evolve into chronic inflammation, a key driver in the development of many rheumatic and autoimmune diseases. The biosynthesis of specialized pro-resolving mediators (SPMs) orchestrates the resolution phase of inflammation, leading to the shutdown of phlogosis, tissue damage repair, and restoration of homeostasis. Dysregulation in SPMs biosynthesis or receptor expression and signalling are related to impaired viruses' clearance and adaptive immune response. Emerging knowledge on the involvement of SPMs in the development and progression of rheumatic diseases is arising. An altered SPM profile has been observed in different rheumatic diseases, including Rheumatoid Arthritis, Systemic Lupus Erythematosus, Adult-onset Still's Disease, Systemic Sclerosis, and Sjögren's Syndrome. Considering the anti-inflammatory and pro-resolving roles of these molecules, the possible use of synthetic SPMs and fish oil supplements, a crucial source of SPMs precursors DHA, DPA and EPA, in patients affected by chronic inflammatory diseases, is emerging.
Monoclonal Gammopathy of Rheumatologic Significance (MGRhS): a systemic vision of clonal disorders with multiple organ involvement.
Quartuccio L, Manfrè V, Treppo E … +4 more , Perrotta F, Ragab G, Goules A, Lubrano E
Autoimmun Rev · 2025 Nov · PMID 40744142 · Publisher ↗
Monoclonal gammopathy (MG) encompasses a spectrum of conditions ranging from benign to malignant clonal B-cell proliferations. While MG is traditionally associated with hematologic malignancies, its role in autoimmune an...
Monoclonal gammopathy (MG) encompasses a spectrum of conditions ranging from benign to malignant clonal B-cell proliferations. While MG is traditionally associated with hematologic malignancies, its role in autoimmune and rheumatologic diseases is increasingly recognized. This review proposes the novel concept of "monoclonal gammopathy of rheumatologic significance (MGRhS)" that refers to a non-malignant or pre-malignant systemic condition related to a monoclonal immunoglobulin and clonal B cells, capable of producing multi-organ damage or influencing the therapeutic management of rheumatologic diseases. MG of clinical significance is characterized by the production of monoclonal proteins causing organ damage and modulating immune responses. These proteins contribute to rheumatologic conditions or peculiar phenotypes, including cryoglobulinemic vasculitis, Sjögren's disease, and other autoimmune disorders. The review explores pathogenic mechanisms linking MG with these diseases, emphasizing early detection and accurate classification to guide therapeutic strategies. The manuscript addresses the implications of incidental MG detection in rheumatologic patients, particularly in the context of biologic therapies. Practical guidance is provided on identifying MGRhS, assessing its impact, and tailoring management to prevent complications. This analysis aims to advance understanding of MGRhS as a distinct clinical entity, encouraging a multidisciplinary approach to its management. The integration of novel diagnostic tools and targeted therapies is essential to improve outcomes and address the complexity of this condition.
Intersecting paths between autoimmunity and bone marrow fibrosis: the case of autoimmune myelofibrosis.
Carubbi F, Alunno A, Matone E … +3 more , Lucchesi A, Musuraca G, Ferri C
Autoimmun Rev · 2025 Nov · PMID 40738294 · Publisher ↗
Bone marrow fibrosis is frequently observed in patients with haematological malignancies including myeloproliferative neoplasm (MPNs). The most common cause of BMF is the BCR-ABL-negative MPN primary myelofibrosis (PMF)...
Bone marrow fibrosis is frequently observed in patients with haematological malignancies including myeloproliferative neoplasm (MPNs). The most common cause of BMF is the BCR-ABL-negative MPN primary myelofibrosis (PMF) however, BMF may also be caused by a variety of non-neoplastic disorders such as infections, endocrine diseases and autoimmune diseases (ADs). Autoimmune myelofibrosis (AIMF) is a type of BMF associated with either a fully blown AD (secondary AIMF) or serological signs of autoimmunity without an overt AD (primary AIMF). Although isolated case reports and case series have been published, AIMF remains a poorly recognized disorder. Therefore, we performed a scoping review and critically appraised the literature on AIMF pathogenesis, diagnosis and treatment with a particular focus on similarities and differences between AIMF and PMF.
Understanding the effects of Janus kinase inhibitors on the cardiovascular system in comparison to main biological DMARDs in rheumatoid arthritis.
Zavoriti A, Miossec P
Autoimmun Rev · 2025 Nov · PMID 40721038 · Publisher ↗
Rheumatoid arthritis (RA) is linked to increased cardiovascular (CV) risk, as is typical for systemic inflammation. The systemic effects of inflammatory cytokines induce vascular dysfunction, leading to thrombosis and ot...
Rheumatoid arthritis (RA) is linked to increased cardiovascular (CV) risk, as is typical for systemic inflammation. The systemic effects of inflammatory cytokines induce vascular dysfunction, leading to thrombosis and other CV diseases. Reducing inflammation should attenuate this risk. For several decades, biologics against a single cytokine, such as TNF inhibitors and IL-6 receptor blockers seem to support this, demonstrating excellent control of RA and reduction of CV events. The Janus kinase inhibitors (JAKi) have been approved more recently. By inhibiting the JAK-STAT pathway, they can simultaneously block the function of multiple cytokines. Unlike biologics, JAKi are associated with increased risk of adverse CV events in high-risk RA patients. This review suggests biological mechanisms that could explain the worse CV outcomes with JAKi compared to biologics. Among the key pro-inflammatory cytokines, IFNγ, IL-6 and IL-23 use directly the JAK-STAT pathway, whereas IL-17, TNF and IL-1β do not, lacking JAK-related receptors. Nevertheless, these non-JAK-dependent cytokines can still influence the JAK-STAT pathway to promote vascular effects in an indirect fashion. Moreover, IL-17 and TNF specifically when combined, exert major pro-coagulant and pro-thrombotic effects on vessels independently of JAKs. As a result, JAKi might not block these pathways and even upregulate them, at high concentrations, leading to increased thrombotic risk. Finally, new research shows that JAKi cannot prevent the increase in adhesion and coagulation molecules as well as the deficiency in physiological anti-coagulant proteins triggered by TNF and IL-17 on endothelial cells. Increased efforts to control CV risk factors are critical in this context.
Primordial and primary prevention in rheumatological diseases: The time has come.
Scagnellato L, Salvato M, Iorio L … +6 more , Moccaldi B, Giollo A, Zanatta E, Padoan R, Ramonda R, Doria A
Autoimmun Rev · 2025 Aug · PMID 40716691 · Publisher ↗
Rheumatological, immune-mediated diseases (RDs) impose a substantial global burden, especially on women of working age, resulting in chronic disability and escalating healthcare utilisation. Despite therapeutic advances,...
Rheumatological, immune-mediated diseases (RDs) impose a substantial global burden, especially on women of working age, resulting in chronic disability and escalating healthcare utilisation. Despite therapeutic advances, the incidence of RDs is rising, and no definitive cure exists. Emerging evidence highlights the potential of early-stage interventions, such as addressing preclinical phases of diseases to delay or prevent disease onset. Modifiable risk factors, such as tobacco use, obesity, diet, infections, mechanical strain, and other environmental exposures (e.g., air pollution and ultraviolet radiation), offer clear targets for intervention. Despite increasing efforts in producing high-quality studies for each rheumatological condition, current evidence supports the global promotion of a healthy lifestyle with a balanced diet, regular physical activity and vaccinations, vitamin D supplementation, and minimisation of excessive infectious, mechanical and psychosocial strain. However, to stimulate stakeholders and policymakers in investing and developing strategies for primary prevention, further interventional trials are warranted on at-risk populations such as first-degree relatives of rheumatological patients and asymptomatic autoantibody carriers. Indeed, besides encouraging experiments in rheumatoid arthritis and psoriatic arthritis, where research has reached the adolescent stage, research in disease interception is still in its infancy for most rheumatological conditions.
Cardiovascular risk in psoriatic arthritis: How can we manage it?
Atzeni F, Rodríguez-Carrio J, Alciati A … +2 more , Tropea A, Marchesoni A
Autoimmun Rev · 2025 Nov · PMID 40712815 · Publisher ↗
It is now widely recognized that patients with psoriatic arthritis (PsA) have a higher risk of cardiovascular disease (CVD) when compared with the general population. A number of factors contribute to this increased risk...
It is now widely recognized that patients with psoriatic arthritis (PsA) have a higher risk of cardiovascular disease (CVD) when compared with the general population. A number of factors contribute to this increased risk. Skin and articular inflammation have been shown to be independently associated with CVD in PsA patients. Metabolic syndrome and all its components are significantly more frequent in PsA patients than in healthy populations. Depression, which is not uncommon in psoriatic subjects, seems to increase the CV risk. Finally, corticosteroids and non-steroidal anti-inflammatory drugs, which are often used for the treatment of PsA, have a well-known pro-atherosclerotic effect. Therefore, in PsA patients the CV risk should be regularly estimated, using validated scoring instruments and appropriate techniques of vascular assessment when needed. Instrument choice and usefulness in PsA populations are still under debate. Patients at high risk should be treated addressing all the risk factors and tightly monitored. Abrogation or, at least, reduction of skin and articular inflammation, appropriate treatment of the metabolic abnormalities, and modifications of unhealthy life habits are the measures that can substantially improve the CV outcome of the patients with PsA. Cooperation of different specialists may be needed to optimize the management of the individual patient. Artificial intelligence applications, novel biomarkers and new care approaches, including treatment strategies and decision-making processes, may be considered in the PsA setting.
Social determinants of health and disparities across the Patient pathway in Systemic Lupus Erythematosus: a narrative review.
Guimarães de Oliveira D, Karakikla-Mitsakou Z, Koskina L … +1 more , Arnaud L
Autoimmun Rev · 2025 Sep · PMID 40706740 · Publisher ↗
OBJECTIVE: Systemic Lupus Erythematosus (SLE) is a complex, chronic autoimmune disease with significant heterogeneity in its presentation and progression. Social determinants of health (SDH), including socioeconomic fact...
OBJECTIVE: Systemic Lupus Erythematosus (SLE) is a complex, chronic autoimmune disease with significant heterogeneity in its presentation and progression. Social determinants of health (SDH), including socioeconomic factors, health literacy and access to care, among others, can shape SLE outcomes. This review explores the impact and interaction of these factors across the entire lupus patient pathway - from presentation to therapeutic management and outcomes - and proposes targeted solutions to improve health equity and patient outcomes in SLE. METHODS: Narrative review, synthesizing findings from peer-reviewed studies published in the last decade, focusing on SDH influencing SLE outcomes. RESULTS: SDH were found to consistently influence the entirety of the SLE patient pathway. Lupus patients from lower socioeconomic backgrounds experience increased diagnostic delay, worse damage accrual and higher mortality rates. Health literacy emerged as a critical factor, with tailored educational interventions shown to improve therapeutic adherence. Geographic disparities were also significant, with persons living in rural areas reporting reduced access to specialist care compared to urban counterparts. Interventions addressing financial barriers, transportation assistance and remote healthcare options demonstrated potential to improve access and outcomes. Additional approaches are proposed, that take into account the intersection of multiple vulnerabilities, their correlation and their interaction with individual lupus characteristics, which result in cumulative effects on disease severity. CONCLUSIONS: Social determinants of health have a profound and measurable impact on SLE outcomes, highlighting the need for multidisciplinary approaches to reduce disparities. Evidence supports targeted interventions aimed at answering local and individual patient contexts, but also multi-level policy changes that address the complexity of these determinants' intersections, to reduce disparities and improve lupus patient outcomes overall. Further studies are critically needed to understand the broader geographic and cultural implications of these social determinants, and longitudinal research should prioritize evaluating the implementation and scalability of strategies addressing these factors.
Exploring vaccine safety and adverse events in major autoimmune diseases.
Sodagari S, Sodagari N
Autoimmun Rev · 2025 Sep · PMID 40706739 · Publisher ↗
This study evaluates post-vaccination adverse events by analyzing a large dataset of patients with major autoimmune diseases, including Hashimoto's n=26,330; Rheumatoid Arthritis n=9,251; psoriasis n=5,589; Systemic Lupu...
This study evaluates post-vaccination adverse events by analyzing a large dataset of patients with major autoimmune diseases, including Hashimoto's n=26,330; Rheumatoid Arthritis n=9,251; psoriasis n=5,589; Systemic Lupus Erythematosus n=4,208; Inflammatory Bowel Disease n=5,831; type 1 diabetes n=2,235; vasculitis n=466; Guillain-Barré Syndrome n=185; Immune Thrombocytopenic Purpura n=623; ankylosing spondylitis n=926; Sjögren's syndrome n=269; psoriatic arthritis n=2,355; polymyositis n=169; dermatomyositis n=130. Our objective is not to refute the importance of vaccines, but to raise awareness about potential risks observed in autoimmune patients by analyzing CDC (Centers for Disease Control and Prevention) data. The sex distribution analysis in vaccine adverse events highlights a consistent female predominance across most autoimmune conditions. We designed machine learning predictive classification models by identifying key predictors to predict severe adverse events (hospitalization or death) following vaccination based on clinical and demographic predictors including age, sex, vaccine type, dose series, and vaccine route. Our models identified distinct risk profiles for severe events across diseases. Example AUC values ranged from 0.90 for dermatomyositis and GBS to 0.98 for Psoriatic Arthritis with accuracy 96% observed for ankylosing spondylitis. Vasculitis and Sjögren's showed peak precision scores, while polymyositis showed peak recall (97%). Moreover, the reported adverse events in the first week and after the 6th week of vaccine administration are one order of magnitude larger than reported incidents in other time intervals for all diseases. Understanding these differences can inform safer vaccination strategies. We recognize the essential public health role of vaccines and underscore the importance of vigilant post-vaccination monitoring in autoimmune populations.
Breast and gynecological cancer risk in systemic lupus erythematosus: A meta-analysis of cohort studies.
Lu Y, Pan H, Wen C … +2 more , Huang L, Li X
Autoimmun Rev · 2025 Nov · PMID 40701373 · Publisher ↗
OBJECTIVE: To evaluate the association between systemic lupus erythematosus (SLE) and the risk of breast and gynecological cancers through a systematic review and meta-analysis of cohort studies. METHODS: A comprehensive...
OBJECTIVE: To evaluate the association between systemic lupus erythematosus (SLE) and the risk of breast and gynecological cancers through a systematic review and meta-analysis of cohort studies. METHODS: A comprehensive search was conducted in PubMed, Embase, and the Cochrane Library. The quality of the studies was assessed using the Newcastle-Ottawa Scale (NOS). Statistical analyses were performed, with separate analyses for standardized incidence ratios (SIRs) and 95 % confidence intervals (CIs). Sensitivity analyses, publication bias assessment using funnel plots and Egger's regression test, and subgroup analyses were conducted. RESULTS: The meta-analysis found no significant association between SLE and risk of breast cancer (SIR = 0.84, 95 % CI 0.64-1.11), I = 97.8 %, P = 0.000) or ovarian cancer (SIR = 0.96, 95 % CI 0.72-1.28, I = 60.9 %, P = 0.003). However, a significant increase in uterine cancer risk was observed (SIR = 1.41, 95 % CI 1.09-1.82, I = 94.3 %, P = 0.000). The strongest association was found for vaginal/vulvar cancer (SIR = 3.61, 95 % CI 2.41-5.41, I = 66.6 %, P = 0.006). Subgroup analyses indicated significant regional variations. European patients showed reduced breast cancer risk (SIR = 0.73, 95 % CI 0.57-0.94), while no significant association was observed in Asian or North American populations. Patients from developed countries had lower ovarian cancer risk than those from developing countries (SIR = 0.82, 95 % CI 0.59-1.60). CONCLUSION: SLE is associated with an increased risk of uterine and vaginal/vulvar cancers, but not with breast or ovarian cancers. Subgroup analyses reveal regional differences in the relationship between SLE and breast/gynecological cancers.
Intersection of immune signaling and cell death: The bidirectional regulatory mechanism of STING pathway and Ferroptosis.
Yao Y, He X, Zhu Y … +9 more , Gong Y, Song X, Chen J, Guo N, Zhao Y, Guo J, Luo X, Zhang X, Huang L
Autoimmun Rev · 2025 Sep · PMID 40692093 · Publisher ↗
The STING signaling pathway is a central component of the innate immune system, primarily responsible for sensing cytosolic DNA and triggering type I interferon responses to regulate innate immune signaling. Recent studi...
The STING signaling pathway is a central component of the innate immune system, primarily responsible for sensing cytosolic DNA and triggering type I interferon responses to regulate innate immune signaling. Recent studies have revealed that, beyond its roles in immune responses, inflammation, and infection, STING can also regulate metabolism and cell death through classical or non-classical signaling pathways. Ferroptosis, a unique iron-dependent form of cell death characterized by intracellular iron accumulation and lipid peroxidation, has been implicated in various diseases, including cancer, autoimmune diseases, neurodegenerative disorders, and infections. Emerging research has demonstrated a correlation between STING and ferroptosis. STING activation induces the production of inflammatory factors and cytokines, which disrupt iron homeostasis, lipid metabolism, and oxidative balance, thereby triggering ferroptosis. Meanwhile, key proteins like GPX4 and ACSL4 in ferroptosis along with certain metabolic products can also influence the activity of the STING signaling pathway. The regulatory direction and signaling intensity of these interactions significantly impact disease states. As a result, deciphering their molecular mechanisms is critical for developing precise therapeutic strategies. Here, we provide a comprehensive overview of the latest research advances related to the STING signaling pathway and ferroptosis, with a particular emphasis on the molecular mechanisms underlying their mutual regulation. In addition, we discuss therapeutic strategies targeting STING signaling and ferroptosis in disease pathology, thereby highlighting their prospective clinical significance in conditions such as cancer and autoimmune diseases.
The assessment and management of bone health in pediatric-onset rheumatological diseases from early age to adulthood: A critical overview.
Di Taranto R, Amati A, Crotti C … +6 more , Baldo F, Costi S, Marino A, Varenna M, Caporali R, Chighizola CB
Autoimmun Rev · 2025 Nov · PMID 40692092 · Publisher ↗
Despite the advancements achieved in modern rheumatology, patients with pediatric-onset rheumatological diseases are still exposed to systemic and/or articular inflammation and corticosteroid treatment, all exerting detr...
Despite the advancements achieved in modern rheumatology, patients with pediatric-onset rheumatological diseases are still exposed to systemic and/or articular inflammation and corticosteroid treatment, all exerting detrimental effects on the growing skeleton together with the reduced body weight and scarce physical activity that rheumatological patients usually experience. The assessment of bone mass in pediatric subjects carries computational limitations: Dual energy X-ray Absiorptiometry (DXA) underestimates bone mineral density (BMD) especially in case of smaller bone, an instance that occurs frequently in children with rheumatologic conditions due to the high rate of short stature or pubertal delay. The rates of low BMD in juvenile idiopathic arthritis (JIA) patients range between 3 % and 34 %, being higher in systemic and polyarticular JIA; patients with juvenile onset systemic lupus erythematosus (jSLE) present a low BMD in approximately 1/3 of cases. Such reduction in BMD presents early on disease course, persists with aging but might be reversed by rheumatological treatment. In pediatric populations, the term osteoporosis should be reserved to children with clinically relevant fractures, favoring "low BMD for chronological age". The prevalence of vertebral fractures ranges between 10 % and 30 % in JIA, peaking in female JIA patients aged 10-15 years, and between 21.4 % and 52 % in jSLE. While calcium and vitamin D supplementation should be optimized in all pediatric patients with rheumatological conditions, bisphosphonates should be reserved to subjects with fragility fractures; the prescription for primary fracture prevention in glucocorticoid-treated children is recommended only in case of a dosage <0.1 mg/kg/day for at least 3 months.
Managing the clinical heterogeneity of patients with Still's disease, from early diagnosis to timely treatment.
Ruscitti P, Cantarini L, Ciccia F … +7 more , Conti F, Dagna L, Iannone F, Montecucco C, Giovanni P, Sfriso P, Giacomelli R
Autoimmun Rev · 2025 Sep · PMID 40684897 · Publisher ↗
Still's disease is an inflammatory syndrome affecting patients across all ages, previously known as systemic juvenile idiopathic arthritis (sJIA) in children and adult-onset Still's disease (AOSD) in adults. Multiple lin...
Still's disease is an inflammatory syndrome affecting patients across all ages, previously known as systemic juvenile idiopathic arthritis (sJIA) in children and adult-onset Still's disease (AOSD) in adults. Multiple lines of evidence reported overlapping clinical features between sJIA and AOSD, commonly manifesting with daily fever, arthritis, evanescent salmon-coloured skin rash. The concomitant various degree of multiorgan involvement may increase the heterogeneity of the patient clinical picture. In active patients, a typical hyperferritinemia is recognized in association with increases of erythrocyte sedimentation rate and C reactive protein. Concerning pathogenesis, also in this case, similar mechanisms are reported in sJIA and AOSD involving both innate and adaptive arms of the immune systems; thus, Still's disease is peculiarly codified at the cross-road of autoinflammatory and autoimmune disorders. Furthermore, life-threatening complications burden the disease course in challenging the management of these patients, mainly macrophage activation syndrome, and worsening the prognosis. Concerning the treatment, glucocorticoids (GCs), conventional synthetic disease-modifying anti rheumatic drugs (csDMARDs) and biologic DMARDs (bDMARDs), mainly IL-1 inhibitors, are administered to treat these patients. Usually, bDMARDs are considered in case of failure of GCs or GC-dependence. However, in some circumstances, bDMARDs may be administered as first-line modifying therapy without GCs, thus avoiding GC predictable side effects and optimizing the long-term outcome. In this work, we aimed to synthetize the recent available literature considering the clinical management of patients with Still's disease, reviewing features about early diagnosis, optimal treatment algorithm, clinical therapeutic targets, treatment of complications, and patient monitoring in the follow-up.
Corrigendum to "Proportion of circulating T follicular helper cells in peripheral blood of systemic lupus erythematosus patients: A systematic review and meta-analysis" [Autoimmunity Reviews Volume 24, Issue 10, 24 September 2025, 103874].
Feng F, Wu Z, Xu H … +2 more , Li Y, Zhang S
Autoimmun Rev · 2025 Sep · PMID 40684610 · Publisher ↗
Abstract loading — click title to view on PubMed.
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