Current Opinion in Immunology最新文献

{"title":"Epigenetics: the link between environmental exposures and autoimmune diseases","authors":"Wenhui Zhou ,&nbsp;Bo Zhang ,&nbsp;Ming Zhao ,&nbsp;Qianjin Lu","doi":"10.1016/j.coi.2025.102592","DOIUrl":"10.1016/j.coi.2025.102592","url":null,"abstract":"<div><div>Autoimmune diseases (AIDs) comprise a highly heterogeneous group of disorders with significant morbidity, disability, and mortality. Growing scientific evidence has suggested the interactions between genetic and environmental factors robustly involving in the pathogenesis of AIDs. Epigenetics serves as a critical bridge linking between gene expression patterns and external environmental stimuli. Several research areas have emerged to investigate these epigenetic modifications, including DNA methylation, histone modifications, and microRNAs. On the other hand, epidemiological studies have well-established the marked relationship between the occurrence and development of AIDs and environmental exposures, especially chemical, physical, and biologic factors. However, the knowledge gap between the role of specific external agents in the development of AIDs and the impact of epigenetic signatures has not been filled. This review synthesizes recent findings AID-associated environmental factors, their role in the development of AIDs, and their interactions with genetics and influence on epigenetic modifications. We also discuss the tool for assessing causal relationships between environmental risks and clinical intervention trials to prevent disease progression. In all, precise understanding of the underlying mechanisms between epigenetics and environmental risk factors is crucial for timely prevention and treatment to improve AIDs outcomes.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102592"},"PeriodicalIF":6.6,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144297402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial overview: Transfusion is not a miracle, but an extraordinary fact and an immunological impossibility","authors":"Olivier Garraud ,&nbsp;Pierre Tiberghien,&nbsp;Fabrice Cognasse","doi":"10.1016/j.coi.2025.102586","DOIUrl":"10.1016/j.coi.2025.102586","url":null,"abstract":"","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102586"},"PeriodicalIF":6.6,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of spatial transcriptomics in psoriasis: new insights into cellular contributions","authors":"Andrea Leung ,&nbsp;Georgia Marquez-Grap,&nbsp;Allison Kranyak,&nbsp;Wilson Liao","doi":"10.1016/j.coi.2025.102585","DOIUrl":"10.1016/j.coi.2025.102585","url":null,"abstract":"<div><div>Spatial transcriptomics (ST) is a technology that has advanced our understanding of the cellular and genetic characteristics of conditions like psoriasis, cancer, and neurodegenerative diseases. ST is often used in conjunction with methods like single-cell RNA sequencing (scRNA-seq), which is a popular method to investigate cellular gene expression. Together, ST and scRNA-seq allow for the visualization and quantification of gene expression spatially, with the preservation of tissue architecture. In psoriasis research, ST and scRNA-seq have led to the identification of distinct cell populations within the skin, associated dysregulated pathways, and critical insight into tissue microenvironments and cell-to-cell interactions. In this review, we provide a summary of how ST has been utilized to better understand psoriasis and how it has shaped our understanding of prominent cell types in psoriasis.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102585"},"PeriodicalIF":6.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144254287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuromodulation by the immune system: implications for brain-directed immunotherapy","authors":"Daniel H Cho ,&nbsp;Jun R Huh ,&nbsp;Gloria B Choi","doi":"10.1016/j.coi.2025.102568","DOIUrl":"10.1016/j.coi.2025.102568","url":null,"abstract":"<div><div>Once believed to be limited in its impact on the brain, the immune system is now recognized as a potent modulator of the brain and behavior. This review explores the evolving understanding of the brain–immune axis, highlighting the role of immune cells and molecules in neuromodulation and behavioral regulation, with a focus on recent findings detailing the influence of immune factors like interleukin (IL)-17A, IL-17E, IL-4, C-C motif chemokine ligand 5, and matrix metalloproteinase 8 on social behavior, learning, memory, and stress susceptibility. The advent of immunotherapy has revolutionized treatments for cancer and autoimmune diseases. Emerging evidence suggests that similar approaches could address neurological and psychiatric disorders by targeting dysregulated brain–immune interactions. A deeper understanding of the complex relationship between the brain and the immune system will be essential for unlocking the therapeutic potential of immunomodulation for brain disorders and positioning the immune system as a key player in restoring mental health.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102568"},"PeriodicalIF":6.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144229960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging role of follicular regulatory T-cells in neuroimmunological disorders","authors":"Stephen Opoku ,&nbsp;Qisen Guo ,&nbsp;Jianmei W Leavenworth","doi":"10.1016/j.coi.2025.102584","DOIUrl":"10.1016/j.coi.2025.102584","url":null,"abstract":"<div><div>Immune tolerance is essential for preventing self-damage while maintaining effective immune responses against foreign insults. Disruptions in this balance contribute to autoimmune and inflammatory conditions, including neuroimmunological disorders that are characterized by aberrant inflammation in the nervous system. Follicular regulatory T (T_FR) cells, a specialized subset of regulatory T (Treg) cells, play important roles in the control of humoral immunity, properly regulating high-affinity antibody responses to foreign antigens while limiting autoreactive antibody production. Beyond this well-documented role, recent studies have revealed its tissue-specific regulation along with the new discoveries of tissue Treg cells. In this review, we focus on the current understanding of T_FR cells and discuss the emerging findings of these cells in neuroimmunological disorders by highlighting their heterogeneity and plasticity in the regulation of disease progression.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102584"},"PeriodicalIF":6.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144213403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Animal models of autoimmune encephalitis","authors":"Estibaliz Maudes ,&nbsp;Jesús Planagumà ,&nbsp;Martin S Weber ,&nbsp;Josep Dalmau","doi":"10.1016/j.coi.2025.102579","DOIUrl":"10.1016/j.coi.2025.102579","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Purpose of the review&lt;/h3&gt;&lt;div&gt;To provide an overview of animal models and mechanisms of autoimmune encephalitides associated with autoantibodies against neuronal surface antigens.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Principal findings&lt;/h3&gt;&lt;div&gt;Currently, 18 encephalitides are known to be mediated by cell-surface autoantibodies, with 16 targeting neuronal proteins or receptors. These diseases, which can affect patients of all ages, are severe but usually respond to immunotherapy. They also serve as valuable models for studying how immune disruptions of neuronal proteins impair memory, behavior, cognition, or lead to psychosis, seizures, or abnormal movements. The process of modeling these diseases involves three steps: (1) demonstrating that patients’ cerebrospinal fluid (CSF) or serum alters the structure or function of the target antigen; (2) confirming that animal transfer of patient-derived CSF, serum IgG, or monoclonal antibodies replicates the molecular effects and disease symptoms; and (3) developing active immunization-based animal models. While passive transfer models are crucial for demonstrating the pathogenicity of patients’ autoantibodies, they have limitations in fully elucidating the neuro-immunobiology of these diseases (e.g. contribution of T-cells, microglia, native immunity, deep cervical lymph nodes). Additionally, these models fall short in evaluating the long-term clinical course and immunological therapies. Active immunization models, currently available only for anti-NMDAR encephalitis, overcome these limitations, capturing the acute and chronic disease course, introducing novel neuroimmunological paradigms, and enabling the assessment of treatment strategies beyond initial immunotherapy.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Although animal models are inherently imperfect, current models of autoimmune encephalitides offer valuable neurobiological and immunological insights, facilitating the translation of experimental findings into clinical advancements.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Key points&lt;/h3&gt;&lt;div&gt;&lt;ul&gt;&lt;li&gt;&lt;span&gt;1.&lt;/span&gt;&lt;span&gt;&lt;div&gt;Antibody-mediated encephalitides provide valuable models for studying how immune disruptions of neuronal proteins or receptors impair memory, behavior, cognition, or cause psychosis, seizures, or abnormal movements.&lt;/div&gt;&lt;/span&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;2.&lt;/span&gt;&lt;span&gt;&lt;div&gt;Modeling autoimmune encephalitides involves three steps: (1) assessing antibody effects on cultured neurons; (2) passively transferring human autoantibodies to animals to evaluate antigen-specific symptoms; and (3) inducing an autoimmune response in animals through immunization with full-length protein or peptide autoantigens.&lt;/div&gt;&lt;/span&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;3.&lt;/span&gt;&lt;span&gt;&lt;div&gt;Passive transfer models are essential for demonstrating autoantibody pathogenicity but are limited by a narrow symptom range, a short duration of effects, and the absence of other components of the immune response (e.g. inflammation, T-cells, microglia).&lt;/div&gt;&lt;/span&gt;&lt;/li&gt;&lt;li&gt;&lt;","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102579"},"PeriodicalIF":6.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144213405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic regulation of B cell response in autoimmune diseases","authors":"Jingjing Chen ,&nbsp;Xiaoming Wang","doi":"10.1016/j.coi.2025.102582","DOIUrl":"10.1016/j.coi.2025.102582","url":null,"abstract":"<div><div>The maintenance of peripheral tolerance depends on various regulatory mechanisms. Thus, the breakdown of self-tolerance leads to the development of autoimmunity. Although the pathogenesis of autoimmune diseases is complex, they are primarily antibody mediated. Notably, autoreactive antibodies are detectable in ∼70% of patients with rheumatoid arthritis and have pathogenic effects. Hence, it is important to investigate the molecular mechanisms underlying B cell response in autoimmune diseases. Recent studies have shed light on the alterations in epigenetic modifications that accompany the development of autoimmune diseases. In this review, we will discuss the recent advances in this field, which may provide precise clues for the diagnosis and therapies for patients with autoimmune disorders.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102582"},"PeriodicalIF":6.6,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted immunotherapy of psoriasis: focusing on Janus kinase/signal transducers and activators of transcription signaling pathway","authors":"Zeyu Chen ,&nbsp;Suyang Lin ,&nbsp;Lian Cui ,&nbsp;Qian Yu ,&nbsp;Yuling Shi","doi":"10.1016/j.coi.2025.102583","DOIUrl":"10.1016/j.coi.2025.102583","url":null,"abstract":"<div><div>Psoriasis is a chronic inflammatory skin condition that affects approximately 1%–3% of the global population. The advent of biologic therapies has markedly improved the management of moderate-to-severe cases. While the efficacy and safety of these novel agents are well documented, many patients value the convenience of oral therapies, which not only eliminate the risk of injection site infections and complications but also alleviate the fear and discomfort associated with needles. The Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling pathway plays a crucial role in mediating the psoriatic inflammatory responses. Current research is focused on developing oral therapies, particularly JAK/STAT inhibitors, that provide improved efficacy and safety. In contrast to existing reviews, our scoping review not only evaluates randomized controlled trials of pan-JAK, selective JAK, and selective tyrosine kinase 2 inhibitors but also delves into mechanistic insights regarding both therapeutic effects and mechanisms of relapse.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102583"},"PeriodicalIF":6.6,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144177420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetics of atopic dermatitis: pathogenesis and therapeutic prospects","authors":"Chi Fang ,&nbsp;Pian Yu ,&nbsp;Jie Li ,&nbsp;Xiang Chen ,&nbsp;Cong Peng","doi":"10.1016/j.coi.2025.102581","DOIUrl":"10.1016/j.coi.2025.102581","url":null,"abstract":"<div><div>Atopic dermatitis (AD) is a chronic inflammatory skin disease that poses a serious threat to human physical and mental health. Its main clinical features include itching, lichenification, and dry skin. The etiology of AD is not yet fully understood, and its pathogenesis is only partially elucidated. An increasing body of evidence suggests that this refractory disease is associated with epigenetic alterations, including specific modifications in immune cells and keratinocytes that play a key role in the pathogenesis of AD. The latest advances in epigenetic research have provided new insights into the pathogenesis of AD and potential therapeutic targets. In this review, we discuss the impact of DNA methylation, noncoding RNAs, and histone modifications on the pathogenesis of AD, emphasizing the potential of epigenetic modifications as targeted biomarkers, which pave the way for the development of novel targeted therapies and personalized medical approaches.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102581"},"PeriodicalIF":6.6,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144177421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can we cure Sjogren’s disease? Unmet needs and raising questions in the era of Precision medicine","authors":"Loukas Chatzis ,&nbsp;Andreas V Goules ,&nbsp;Athanasios G Tzioufas","doi":"10.1016/j.coi.2025.102578","DOIUrl":"10.1016/j.coi.2025.102578","url":null,"abstract":"<div><div>The wide spectrum of Sjögren's disease (SjD) clinical manifestations coupled with its multifaceted pathogenesis has complicated drug target development, optimal clinical trial design, identification of suitable SjD subgroups, selection of appropriate outcome measures, and interpretation of treatment efficacy. Despite recent advancements in biologic treatments for autoimmune diseases, the targeted therapy(ies) for SjD remain an unmet need, with no regulatory approvals, so far. Recent large, randomized studies have suggested some patient benefits; however, reproducibility is needed, and assessment of treatment efficacy requires refinement. In this review, we explore the potential for curing SjD taking into consideration the main pathogenetic mechanisms, clinical phenotypes, and underlying endotypes. We provide an overview of current recommendations and targeted treatments, identify potential reasons for treatment failures, and propose strategies (in and out of the box) for future directions. By addressing these areas, we offer a comprehensive perspective that may inform future research and therapeutic strategies for SjD.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"95 ","pages":"Article 102578"},"PeriodicalIF":6.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144177489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}