Autoimmunity reviews最新文献

{"title":"Causation-based SLE diagnostic criteria should replace advance-repressing SLE classification criteria","authors":"Ole Petter Rekvig ,&nbsp;George C. Tsokos","doi":"10.1016/j.autrev.2026.103990","DOIUrl":"10.1016/j.autrev.2026.103990","url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) presents with diverse clinical manifestations originating from multiple contributing factors employing a complex array of pathogenetic pathways. Understanding the origin of the disease is stifled by the assumption that a set of classification criteria represent one disease. Efforts to continuously refine the SLE classification criteria over the last 50 years have been based on the assumption that they will solve core aspects of SLE. Yet, this optimism has failed to deliver, because it is not possible to conquer a complex disease through criteria which are arbitrarily selected, but not supported by causal mechanisms. We propose to reconsider the value of SLE classification criteria and contemplate the development of diagnostic criteria directed by causality to bolster research and treatment efforts. This communication proposes that SLE diagnostic criteria should replace SLE classification criteria, at which point SLE will be studied within the context of causality. Such an accomplishment will optimize SLE research and the care of patients with SLE.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 103990"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146103535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imaging the hidden player: Choroid plexus enlargement in multiple sclerosis","authors":"Antonio Daniel Corlatescu ,&nbsp;Horia Petre Costin ,&nbsp;Gabriel González-Escamilla ,&nbsp;Sergiu Groppa ,&nbsp;Vinzenz Fleischer","doi":"10.1016/j.autrev.2026.104001","DOIUrl":"10.1016/j.autrev.2026.104001","url":null,"abstract":"<div><div>The choroid plexus (CP), one key regulator of cerebrospinal fluid (CSF) production and immune surveillance at the blood–CSF barrier, has recently emerged as a relevant structure in multiple sclerosis (MS) pathophysiology. This review synthesizes current evidence highlighting CP enlargement as measured with magnetic resonance imaging (MRI) as a potential biomarker of neuroinflammation and neurodegeneration in MS. We first outline the basic immunological roles of the CP, emphasizing its function as a dynamic interface facilitating immune cell trafficking and cytokine production within the CNS. Advances in MRI and PET (positron emission tomography) imaging have enabled the quantification of CP volume, revealing enlargement across different MS stages, including radiologically isolated syndrome and pediatric MS. CP volume correlates with lesion load, chronic lesion expansion, microglial activation, and inflammatory CSF profiles, suggesting its responsiveness to neuroinflammatory activity. Notably, CP enlargement is also associated with neurodegenerative processes, including gray matter atrophy, cognitive decline, and disability progression, indicating its potential role also as a surrogate marker of MS-related neurodegeneration. However, methodological variability, confounding factors and a lack of longitudinal standardization challenge the interpretation of CP metrics. We highlight the need for multimodal approaches to unravel the temporal and mechanistic significance of CP enlargement. Future research should also explore CP-targeted interventions and their relevance for MS progression. Overall, CP imaging, in particular its enlargement, offers a novel, biologically meaningful perspective into MS pathogenesis, bridging inflammatory and degenerative pathways, and holds promise for improved disease monitoring.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 104001"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146155736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obstetric antiphospholipid syndrome: Advances in pathogenesis","authors":"Shumin Wang ,&nbsp;Huimin Liu ,&nbsp;Wanrong Huang ,&nbsp;Xun Zeng ,&nbsp;Lang Qin ,&nbsp;Rui Gao","doi":"10.1016/j.autrev.2026.104013","DOIUrl":"10.1016/j.autrev.2026.104013","url":null,"abstract":"<div><div>The publication of the 2023 ACR-EULAR classification criteria for antiphospholipid syndrome (APS) has shifted the understanding of APS from a “one-size-fits-all” approach to a more nuanced, subphenotype-based research and management paradigm. Obstetric APS (OAPS), characterized by obstetric clinical manifestations, represents a distinct subtype with unique underlying pathophysiology. OAPS is now recognized as a multifactorial autoimmune disorder, extending beyond the previously held view that it is solely caused by placental vascular thrombosis or micro-thrombosis. Recent evidence has confirmed that trophoblast dysfunction, inflammation and decidual microenvironmental dysfunction are also critical in the pathogenesis of OAPS. Looking forward, a comprehensive summary of the pathogenesis of OAPS will facilitate progress in both research and clinical management of this condition.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 104013"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial transfer and transplantation in the immune cells: Mechanistic foundations, medical applications, and future prospects","authors":"Xiaofeng Liu ,&nbsp;Xinyu Feng ,&nbsp;Deping Zhan ,&nbsp;Heng Yin","doi":"10.1016/j.autrev.2026.104011","DOIUrl":"10.1016/j.autrev.2026.104011","url":null,"abstract":"<div><div>Mitochondria exhibit tissue-specific physiological functions and are central to the maintenance of cellular homeostasis. Emerging evidence indicates that intercellular mitochondrial transfer is regulated by multiple determinants and exerts a profound influence on the function of both innate and adaptive immune cells. The underlying mechanisms are highly heterogeneous, involving distinct cellular contexts, microenvironmental cues, and modes of intercellular communication. This review summarizes the major triggers and mechanistic pathways governing mitochondrial transfer in immune cells and immune-related diseases, and discusses the therapeutic potential of this process while highlighting key challenges that currently limit its clinical translation. By integrating recent mechanistic insights and translational perspectives, this review aims to provide a conceptual framework for the development of mitochondrial transfer–based strategies in the treatment of immune-mediated disorders.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 104011"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmunity in the era of immune checkpoint inhibitors: the evolving epidemiology of autoimmune diseases and the possible impact of COVID-19","authors":"Naim Mahroum ,&nbsp;Abdulrahman Elsalti ,&nbsp;Mohamed Alsharif ,&nbsp;Abdullah Jabri ,&nbsp;Abderrahman Ouban","doi":"10.1016/j.autrev.2026.104002","DOIUrl":"10.1016/j.autrev.2026.104002","url":null,"abstract":"<div><div>Immune checkpoint inhibitors (ICIs) have markedly improved the prognosis of previously fatal malignancies, as evidenced by substantial gains in overall and progression-free survival in multiple clinical trials. The mechanism of action of ICIs is based on altering the immune response while the reported side effects display clear autoimmune features. Designated as immune-related adverse events (irAEs) affect nearly every organ system, including the gastrointestinal tract, liver, and thyroid gland, and share features with autoimmune disorders of the same organs. The severity of irAEs ranges from mild to life-threatening reactions. Many cases require systemic corticosteroids, hospitalization, and in many instances the discontinuation of ICI therapy. In this review, we present the history of ICIs, their indications, and the reported irAEs in a systematic manner. We then focus on the autoimmune nature of these side effects, with particular attention to the epidemiology of autoimmune diseases, including their female preponderance in certain age groups. In the final sections, we discuss how irAEs may be altering the epidemiology of autoimmune disease and address the possible effect of COVID-19 as a potential trigger.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 104002"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146155756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heavy and trace metals toxicity implications in the breakdown of cellular homeostasis: A risk factor for rheumatoid arthritis pathogenesis","authors":"Nemat Ali ,&nbsp;Ali M. Alaseem ,&nbsp;Md. Meraj Ansari ,&nbsp;Shambhu Kumar ,&nbsp;Mohammad Suhail Akhter ,&nbsp;Mohammad Fareed ,&nbsp;Prawez Alam ,&nbsp;Glowi Alasiri","doi":"10.1016/j.autrev.2026.104003","DOIUrl":"10.1016/j.autrev.2026.104003","url":null,"abstract":"<div><div>Occupational and environmental exposure to heavy and trace metals is increasingly implicated in cellular dysfunction underlying the pathogenesis of rheumatoid arthritis (RA). While trace metals such as selenium (Se), zinc (Zn), and copper (Cu) are essential for the regulation of immune and inflammatory responses, excessive or imbalanced exposure can disrupt physiological homeostasis. In contrast, exposure to heavy metals including lead (Pb), mercury (Hg), cadmium (Cd), and nickel (Ni) poses significant risks to joint health and has been increasingly associated with progressive joint tissue deterioration. Accumulating evidence indicates that metal-induced toxicity disrupts cellular homeostasis by promoting reactive oxygen species (ROS)-mediated oxidative stress and impairing key cellular processes, including apoptosis, ferroptosis, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress. Moreover, heavy metals may interfere with the autophagy–lysosomal pathway, a critical mechanism for maintaining cellular integrity and immune balance. This review underscores the importance of understanding the complex interactions between heavy and trace metal exposure and their roles in cellular dysfunction and joint tissue degeneration. Elucidating the molecular mechanisms underlying metal-induced toxicity is essential for the development of targeted therapeutic strategies and effective preventive interventions aimed at mitigating RA progression.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 104003"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated lipid peroxidation biomarkers in autoimmune diseases: A systematic review and meta-analysis","authors":"Yixiang Luo ,&nbsp;Siqi Hua ,&nbsp;Tongtong Song,&nbsp;Mingxin Cao,&nbsp;Shuangshuang Song,&nbsp;Shentong Fang,&nbsp;Bo Zhu","doi":"10.1016/j.autrev.2026.104008","DOIUrl":"10.1016/j.autrev.2026.104008","url":null,"abstract":"<div><h3>Background</h3><div>Ferroptosis, an iron-dependent cell death pathway driven by lipid peroxidation (LPO), is implicated in the pathogenesis of autoimmune diseases (AIDs). However, comprehensive clinical evidence establishing the association between specific LPO biomarkers and AIDs is lacking.</div></div><div><h3>Objective</h3><div>To systematically evaluate the clinical evidence for elevated LPO in major AIDs through a meta-analysis, focusing on key biomarkers including malondialdehyde (MDA) and 8-iso-prostaglandin F2α (8-iso-PGF2α).</div></div><div><h3>Methods</h3><div>We searched four databases for studies reporting serum, plasma, or urinary LPO levels in patients with AIDs and healthy controls. Standardized mean differences (SMDs) were pooled using a random-effects model.</div></div><div><h3>Results</h3><div>Across 175 studies (8227 patients; 6866 controls), serum/plasma MDA levels were significantly elevated in all ten investigated AIDs: rheumatoid arthritis (RA) (SMD = 2.82), systemic sclerosis (SSc) (SMD = 2.08), Graves' disease (GD) (SMD = 1.92), Behçet's disease (BD) (SMD = 1.90), Crohn's disease (CD) (SMD = 1.71), multiple sclerosis (MS) (SMD = 1.52), psoriasis (PsO) (SMD = 1.44), ulcerative colitis (UC) (SMD = 1.32), systemic lupus erythematosus (SLE) (SMD = 1.20) and type 1 diabetes mellitus (T1DM) (SMD = 1.12). Disease-specific elevations were found for serum/plasma 8-iso-PGF2α and 4-hydroxynonenal in RA, urinary 8-iso-PGF2α in SSc and T1DM, and serum/plasma oxidized low-density lipoprotein in T1DM. MDA was higher in active or severe subgroups, with significant between-subgroup differences in GD and PsO.</div></div><div><h3>Conclusion</h3><div>This meta-analysis provides robust, large-scale clinical evidence that elevated lipid peroxidation is a common feature across diverse AIDs. These findings solidify the clinical relevance of ferroptosis, positioning LPO products as promising biomarkers and underscoring the therapeutic potential of targeting ferroptosis in autoimmune conditions.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 104008"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146218436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sarcoidosis: Disease mechanisms, diagnostic pathway and treatment","authors":"Jelle Miedema ,&nbsp;Hilario Nunes ,&nbsp;Virgil A.S.H. Dalm ,&nbsp;Marc A. Judson ,&nbsp;Paolo Spagnolo","doi":"10.1016/j.autrev.2026.103993","DOIUrl":"10.1016/j.autrev.2026.103993","url":null,"abstract":"<div><div>Sarcoidosis is an inflammatory granulomatous disease that affects people worldwide and can involve virtually any organ but most commonly the lungs and thoracic lymph nodes. The cause of sarcoidosis remains unknown, but occupational and environmental exposures, genetic background, and ethnicity are likely contributors to disease development. Recent immunological studies, including single-cell RNA sequencing and spatial transcriptomics, have increased our understanding of disease pathogenesis. Diagnosing sarcoidosis is often challenging due to the lack of a diagnostic gold standard and the remarkable variability in clinical presentation. Accordingly, the diagnosis requires the presence of compatible clinical and radiological features along with histopathological evidence of noncaseating granulomas and exclusion of other granulomatous diseases. The differential diagnosis includes infection, drug-induced granulomatosis, inborn error of immunity, vasculitis and malignancies.</div><div>Sarcoidosis often resolves spontaneously, but it is not a benign disease. Up to one-third of patients develops chronic or progressive disease, which carries an increased risk of organ failure or death. Treatment is not always required, but is clearly indicated for progressive pulmonary disease, symptomatic cardiac or central nervous system involvement, and significantly impaired quality of life. Treatment aims to decrease symptom burden and preserve organ function. Corticosteroids have been considered first-line treatment for decades, but their long-term use is associated with substantial toxicity. Recently, methotrexate was found to be equally effective as prednisone as first-line treatment in pulmonary sarcoidosis. The identification of novel pathways involved in disease pathogenesis has suggested JAK inhibitors and mTOR inhibitors as potential therapies. More efficacious and better tolerated therapies are urgently needed; however, the rarity of the disease, its heterogeneous clinical course and the lack of prognostic biomarkers make it difficult to design and implement clinical trials of novel therapies.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 103993"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk of infection for different B-cell targeting agents in treating systemic lupus erythematosus: A systematic review and network meta-analysis","authors":"Zhibin Yu ,&nbsp;Yuxiang Lin","doi":"10.1016/j.autrev.2026.103987","DOIUrl":"10.1016/j.autrev.2026.103987","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to assess the risk of infections in the treatment of systemic lupus erythematosus (SLE) with various B-cell targeting agents.</div></div><div><h3>Methods</h3><div>We systematically searched PubMed, Web of Science, Cochrane Library, and Embase for randomized controlled trials (RCTs) of B-cell targeting agents for SLE as of March 1, 2025. The risk of bias was assessed using Cochrane and NIH tools. The main outcomes were total and serious infections. We performed traditional (TMA) and network meta-analyses (NMA). The risk ratios (RRs) with 95% confidence intervals (CIs) or credible intervals (CrIs) were calculated.</div></div><div><h3>Results</h3><div>A total of 26 studies with 16,338 patients were included, involving 12 B-cell targeting agents. Overall, B-cell targeting therapy did not significantly increase the risk of infections. Nonetheless, obinutuzumab was associated with a greater risk of infections in patients with lupus nephritis compared to placebo (RR [95% CrI] = 1.18 [1.03, 1.37]) and rituximab (RR [95% CrI] = 1.25 [1.04, 1.53]). It was also associated with an elevated risk of infections in the combined population compared to placebo (RR [95% CrI] = 1.18 [1.03, 1.36]), rituximab (RR [95% CrI] = 1.22 [1.04, 1.43]), and epratuzumab (RR [95% CrI] = 1.24 [1.06, 1.45]). BAFF/APRIL-targeting agents showed a higher risk of infections than anti-CD22 agents (only epratuzumab) (RR [95% CrI] = 1.16 [1.01, 1.34]). Low-dose therapy also showed a notably increased risk compared to placebo (RR [95% CrI] = 1.05 [1.00, 1.10]). No significant increase in the risk of serious infections was found.</div></div><div><h3>Conclusions</h3><div>Specific B-cell targeting therapies may modestly increase the risk of total infections.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 2","pages":"Article 103987"},"PeriodicalIF":8.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sporadic late-onset nemaline myopathy (SLONM): Data from a case series and literature review of 144 patients","authors":"Antonio Lauletta ,&nbsp;Francesca Forcina ,&nbsp;Gioia Merlonghi ,&nbsp;Laura Fionda ,&nbsp;Luca Leonardi ,&nbsp;Rocco Costanzo ,&nbsp;Laura Tufano ,&nbsp;Elena Rossini ,&nbsp;Demetrio Marando ,&nbsp;Valentina Vera ,&nbsp;Giovanni Antonini ,&nbsp;Stefania Morino ,&nbsp;Matteo Garibaldi","doi":"10.1016/j.autrev.2025.103960","DOIUrl":"10.1016/j.autrev.2025.103960","url":null,"abstract":"<div><div>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).</div><div>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.</div><div>Of the 144 patients analyzed, 47 % were classified as SLONM-MGUS. These patients exhibited more severe clinical manifestations, including increased respiratory involvement (<em>p</em> = 0.006). Histopathologically, SLONM-MGUS revealed more prominent nemaline rods (<em>p</em> = 0.032), often accompanied by cytoplasmic bodies and lobulated fibers, and frequently required repeat muscle biopsies for diagnosis (<em>p</em> = 0.0285). Inflammatory infiltrates were less frequent in SLONM-MGUS (<em>p</em> = 0.0176). Functional outcomes were significantly worse in this group, with reduced likelihood of full recovery (<em>p</em> = 0.013) and higher rates of non-ambulatory status (<em>p</em> = 0.01).</div><div>Patients receiving dual or more treatment regimens, particularly those including IVIg and/or autologous stem cell transplantation (ASCT), had more favorable outcomes.</div><div>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.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 2","pages":"Article 103960"},"PeriodicalIF":8.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145572848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}