Immunology letters最新文献

{"title":"Tissue resident memory B cells mediate protective immunity to respiratory pathogens in the airways","authors":"Ivy M. Akehurst,&nbsp;Louisa K. James","doi":"10.1016/j.imlet.2025.107091","DOIUrl":"10.1016/j.imlet.2025.107091","url":null,"abstract":"<div><div>Respiratory pathogens pose a significant risk to public health and are responsible for burdening health care by causing worldwide morbidity and mortality. The immune environment in the airway is critical for protection from respiratory pathogens and comprises several specialist subsets of resident lymphocytes and myeloid cells. Tissue resident-memory B cells (B_RM) are a subset of memory B cell which reside in mucosal tissues, including the airways. Although, B_RM have only recently been characterised, they have a crucial role in generating robust and localised immune responses to respiratory infections, particularly secondary responses, by rapidly differentiating into antibody-secreting cells. A greater understanding of their role in protecting the airways from respiratory pathogens will enable the development of immunisation strategies against respiratory disease. This mini-review aims to summarise the current knowledge of B_RM and highlight areas for future research.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107091"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunological features driving distinct repigmentation patterns in patients with stable vitiligo submitted to the autologous keratinocyte/melanocyte transplantation","authors":"Bruna Estefânia Diniz Frias ,&nbsp;Roberta Oliveira Prado ,&nbsp;Mariana Gontijo Ramos ,&nbsp;Nathália Werneck Cézar de Oliveira ,&nbsp;Fernanda Fortes de Araújo ,&nbsp;Liliane Martins dos Santos ,&nbsp;Camila Gontijo Ramos ,&nbsp;Camila Bechara Kallás ,&nbsp;Maria Sílvia Laborne Alves de Sousa ,&nbsp;Ismael Artur Costa-Rocha ,&nbsp;Joaquim Pedro Brito-de-Sousa ,&nbsp;Rachel Basques Caligiorne ,&nbsp;Marcelo Antônio Pascoal-Xavier ,&nbsp;Vanessa Peruhype-Magalhães ,&nbsp;Daniel Gontijo Ramos ,&nbsp;Andréa Teixeira-Carvalho ,&nbsp;Olindo Assis Martins-Filho","doi":"10.1016/j.imlet.2025.107098","DOIUrl":"10.1016/j.imlet.2025.107098","url":null,"abstract":"<div><div>This study aimed to characterize biomarkers of therapeutic response in patients with stable vitiligo undergoing the autologous non-cultured keratinocyte/melanocyte transplantation. The approaches performed were systemic analysis evaluated during pre-transplantation/(D0), seven/(D7), and 28 or more/(D28–45) days after the procedure and compartmentalized analysis in epidermal cell suspension (explant). Increased number of pro-inflammatory monocytes and NK-cells was found during the transplantation follow-up in vitiligo patients compared to the control. There were higher numbers of CD8⁺ <em>T</em>-cells and CD4⁺HLA-DR⁺ <em>T</em>-cells circulating at D28–45 compared to D0, and increased number of CD8⁺HLA-DR⁺ <em>T</em>-cells at D28–45 compared to D7. Decreased levels of the most pro-inflammatory chemokines/cytokines during post-transplantation kinetics timeline were observed. Integrative analysis demonstrated that patients with unsatisfactory repigmentation presented higher numbers of connections between the blood/skin components at D0. The data suggest differentiated profiles in the dynamics of the hematological/immunological biomarkers, according to the kinetics timeline and the clinical outcome of repigmentation in vitiligo patients.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107098"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Restoration of Fli1 expression as a potential therapeutic approach in Systemic Sclerosis: Effects on age-associated B cells","authors":"Athanasios Sachinidis ,&nbsp;Malamatenia Lamprinou ,&nbsp;Theodoros Dimitroulas","doi":"10.1016/j.imlet.2025.107094","DOIUrl":"10.1016/j.imlet.2025.107094","url":null,"abstract":"<div><div>Fli1 is a transcription factor playing a major role in the regulation of normal hematopoiesis and vasculogenesis. Its deficiency has been associated with the development of fibrosis in various diseases, including systemic sclerosis/scleroderma (SSc), a rare autoimmune rheumatic disease. In addition, in <em>Fli1</em> B cell conditional knockout mice, a striking increase of age-associated B cells (ABCs) has been observed. These cells constitute a CD11c⁺CD21^low/- B cell population that displays an expansion in autoimmunity and drives disease pathogenesis. The exact role and functions of ABCs, though, are not yet fully understood. Taking into consideration all the above, regarding Fli1 deficiency in SSc pathogenesis and ABC expansion, we propose restoration of this specific transcription factor’s expression as a potential therapeutic approach for the aforementioned rheumatic disease. Moreover, we provide some interventions that aim to restore Fli1 expression via modulating the signals of TGF-β pathway, whose activation is considered as crucial for fibrosis development in SSc.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107094"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental determinants of immune tolerance in asthma and allergy","authors":"Piia Karisola ,&nbsp;Harri Alenius","doi":"10.1016/j.imlet.2025.107102","DOIUrl":"10.1016/j.imlet.2025.107102","url":null,"abstract":"<div><div>Prevalence of allergic diseases has increased globally, reflecting environmental and behavioral changes. The exposome concept encompasses cumulative chemical, microbial, nutritional, psychosocial, and physical exposures across the life course, offering a unifying framework to understand how immune tolerance is shaped or disrupted. Emerging evidence highlights that early-life exposures are particularly critical. Pollutants, endocrine disruptors, microbial deprivation, dietary shifts, and psychosocial stress contribute to barrier dysfunction, dysbiosis, and immune dysregulation, favoring Th2 dominance and allergy development. In contrast, exposures that enhance biodiversity, microbial diversity, pollution-free air, and balanced nutrition support active tolerance development, especially via regulatory T cells. Mechanistic insights point to the barrier–microbiota–immune axis as central pathways linking the environment to allergic outcomes. Translational studies, including biodiversity enrichment interventions, maternal and infant dietary strategies, and microbiome-based therapies, illustrate the potential of exposome-informed approaches to allergy prevention. However, major challenges remain in measuring complex exposure mixtures, identifying causal pathways, and integrating exposome data with systems immunology. This review synthesizes current knowledge on how the exposome modulates immune tolerance and outlines future research directions toward precision prevention. A deeper understanding of these interactions is essential to address the rising global allergy burden.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107102"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning in allergy research: A bibliometric review","authors":"Ellen Kong ,&nbsp;Alex Cucco ,&nbsp;Adnan Custovic ,&nbsp;Sara Fontanella","doi":"10.1016/j.imlet.2025.107088","DOIUrl":"10.1016/j.imlet.2025.107088","url":null,"abstract":"<div><div>The emergence of big data and analytic approaches initiated research efforts to characterise different subtypes of allergic diseases, including tracking disease progression and identifying patterns that may offer insight into their development and progression. Triangulation from different data sources and study types may help to elucidate the directionality of relationships between variables at a very individual level by modelling the complex interdependencies between multiple dimensions (e.g., genome, transcriptome, epigenome, microbiome, and metabolome), thereby moving away from associative to a more causal analysis. To ascertain the role of machine learning in allergy research, we conducted a comprehensive systematic review of the current literature. The findings highlight and underscore the potential of using AI/ML approaches in advancing our understanding of allergic diseases, which ultimately enhances patient care through improved prevention, diagnosis, and management strategies. It is important to emphasise that there is no single ‘best’ analytical method, highlighting the importance of cross-disciplinary collaborations. A team science approach is crucial for ensuring the application of appropriate methodologies tailored to the research question at hand and that context-specific interpretations are being made, supported by critical appraisal from both the front- (e.g., clinicians) and back-end (e.g., analysts) of research processes.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107088"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota analysis revealed unique biomarkers in Ankylosing Spondylitis and Non-radiographic Axial Spondyloarthritis","authors":"Sijie Chang ,&nbsp;Mingrong Chen ,&nbsp;Peiguang Niu ,&nbsp;Jinhua Zhang","doi":"10.1016/j.imlet.2025.107082","DOIUrl":"10.1016/j.imlet.2025.107082","url":null,"abstract":"<div><h3>Objectives</h3><div>In this paper, the different characteristics of gut microbiota between Ankylosing Spondylitis (AS), Healthy Control (HC), and Non-radiographic Axial Spondyloarthritis (nr-axSpA) were studied. The AS-nr-axSpA differentiation model was constructed to identify patients with these two phenotypes and help doctors make accurate diagnosis.</div></div><div><h3>Methods</h3><div>Stool samples and blood samples of AS, nr-axSpA, and HC were collected from our hospital. Bacterial lipopolysaccharides and lipopolysaccharides-binding proteins in blood were detected by enzyme-linked immunosorbent assay (ELISA). The V3-V4 region of bacterial 16SrRNA was analyzed by MiSeq PE300 sequencing platform with high throughput. Software such as QIIME, R, Excel, etc. were used for statistical analysis of the data. Random Forest (RF) and Area Under Curve (AUC) methods were used to construct the AS-nr-axSpA differentiation model and identify relevant important markers. Set markers and use the receiver operating characteristic curve (ROC) to judge the accuracy of the model.</div></div><div><h3>Results</h3><div>We studied a total of 59 fecal and corresponding blood samples from 31 AS, 21 nr-axSpA, and 7 HC. There was a significant difference in intestinal α diversity between AS and nr-axSpA patients (Shannon index, <em>P</em> = 0.017). Compared to the nr-axSpA patient population, Streptococcus (<em>P</em> = 0.045), Actinomyces (<em>P</em> = 0.0028), Rothia (<em>P</em> = 0.042), and Oribacterium in the intestinal tract of AS patients <em>P</em> = 0.044) increased significantly. However, Dorea (<em>P</em> = 0.034) and Odoribacter (<em>P</em> = 0.043) were significantly reduced. The AS-nr-axSpA model was constructed using 18 factors including Actinomyces and Odoribacter. ROC analysis was performed on the model and an ROC curve was drawn, with an AUC of 0.78, which is moderate accurate.</div></div><div><h3>Conclusions</h3><div>The gut microbiota of patients with AS differs from that of patients with nr-axSpA. The disturbance of gut microbiota may be one of the conditions for the progression of nr-axSpA to AS. The characteristics of gut microbiota and related bacterial products may serve as characteristic factors for differentiating the phenotypes of these two diseases. The AS-nr-axSpA model may help doctors distinguish patients with different phenotypes, but more robust prospective and standardized studies are needed to confirm these findings.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107082"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro analysis of azithromycin’s effect on J774 murine macrophages challenged with Aspergillus fumigatus","authors":"Ivy Antwi,&nbsp;Jarrod R. Fortwendel,&nbsp;Theodore J. Cory","doi":"10.1016/j.imlet.2025.107087","DOIUrl":"10.1016/j.imlet.2025.107087","url":null,"abstract":"<div><h3>Background</h3><div>Patients with chronic lung diseases often suffer from pulmonary aspergillosis, caused by <em>Aspergillus fumigatus</em> (AF). Alveolar macrophages play a key role in the initial immune response to AF. Azithromycin (AZM), commonly known for its immunomodulatory properties in reducing exacerbations and improving lung function, has mixed effects on the development of aspergillosis. While some studies suggest AZM aids AF-colonized patients, others indicate increased rates of AF colonization.</div></div><div><h3>Objective</h3><div>Given AZM's positive impact on host response to other pathogens, we hypothesized that it would improve immune responses to AF by modulating macrophage function. We investigated the in vitro effect of AZM on J774 murine macrophage response to <em>Aspergillus fumigatus.</em></div></div><div><h3>Method</h3><div>The murine macrophage cell line J774 was polarized into distinct phenotypes: (1) classical M1 macrophages, generated using interferon-gamma (IFN-γ) and lipopolysaccharide (LPS); (2) azithromycin-treated M1 macrophages (hereafter referred to as M1A macrophages), generated by treating M1 cells with azithromycin in addition to IFN-γ and LPS; and (3) alternatively activated M2 macrophages, generated using interleukin-4 (IL-4), interleukin-13 (IL-13), and LPS. These polarized macrophages were then analyzed for cytokine production, fungal killing capacity, and reactive oxygen species (ROS) generation.</div></div><div><h3>Results</h3><div>We observed a shift in macrophage phenotype toward an anti-inflammatory-like profile in the AZM-treated group, characterized by an increased fungal killing compared to both M1- and M2-polarized groups. This was accompanied by a reduction in interleukin-6 (IL-6) cytokine production, an increase in arginase activity, without any significant change in ROS generation. Further assays confirmed that the observed increase in fungal clearance was attributable to AZM’s impact on macrophages rather than any direct antifungal activity against <em>Aspergillus fumigatus.</em></div></div><div><h3>Conclusion</h3><div>These findings suggest AZM enhances macrophage function, boosting anti-inflammatory responses and improving fungal clearance.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107087"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Yo antibody associated axial movement disorders – a novel phenotype in ANNS","authors":"Ajith Cherian ,&nbsp;Divya K P ,&nbsp;Amod R ,&nbsp;Deepa K P","doi":"10.1016/j.imlet.2025.107109","DOIUrl":"10.1016/j.imlet.2025.107109","url":null,"abstract":"<div><h3>Background</h3><div>Movement disorders, as an anti-neuronal antibody mediated neurological syndrome(ANNS), is usually associated with anti-CV2/CRMP5,Hu/ANNA1 and Contactin-associated protein-like 2 (CASPR2) antibodies. Anti-Yo antibody associated movement disorders are extremely rare.</div></div><div><h3>Methods</h3><div>We analysed the data of 47 patients with anti –Yo antibodies who presented over a period of 5 years (2019–2024) in a tertiary care institute. Those with movement disorder phenotype, without ataxia, were included. Other etiologies were excluded with relevant work up.</div></div><div><h3>Results</h3><div>We report two elderly males in their sixties who presented with a subacute onset isolated progressive axial movement disorders, with positive anti-Yo antibody. One patient with axial myoclonus and camptocormia who did not initially respond to intravenous methylprednisolone had remarkable improvement with intravenous immunoglobulin and rituximab, while in the other treatment response was suboptimal.</div></div><div><h3>Conclusion</h3><div>Movement disorders due to anti-neuronal antibodies should be suspected when they develop subacutely, in older patients (&gt; 50 years), have a progressive course beyond 3 months, associated with pain and constitutional symptoms like weight loss, all of which were present in our cases. Such intracellular Yo antigen induced ANNS usually have guarded response to immunomodulatory therapy compared to those mediated by antibodies against surface antigens, though one patient of ours had a remarkable improvement.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107109"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145481997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty acid binding protein 2 (FATP2/SLC27A2) blockade with Lipofermata elicits dual effects on inflammatory responses in human monocytes and macrophages","authors":"Nico Hahn ,&nbsp;Serhii Chornyi ,&nbsp;Daan Heister ,&nbsp;Helga E. de Vries ,&nbsp;Martin Giera ,&nbsp;Mariëtte R. Boon ,&nbsp;Gijs Kooij ,&nbsp;Jan Van den Bossche","doi":"10.1016/j.imlet.2025.107092","DOIUrl":"10.1016/j.imlet.2025.107092","url":null,"abstract":"<div><div>Inflammatory responses often involve metabolic rewiring within immune cells to support effector functions. Targeting metabolic pathways in immune cells therefore represents a promising strategy to modulate inflammatory diseases and improve therapeutic outcomes. Acyl-CoA synthesis by fatty acid transporter 2 (FATP2/SLC27A2) facilitates the transport of long-chain fatty acids into the cell. It represents a key step in fatty acid metabolism and the subsequent production of bioactive lipid mediators (LMs) with immunoregulatory functions. While the FATP2 inhibitor Lipofermata is currently evaluated for lipid-lowering therapies in metabolic diseases, and to revert the suppressive nature of myeloid cells in cancer, its effect on inflammatory responses in human macrophages remains elusive.</div><div>Here, we show that Lipofermata reduced LPS-induced inflammatory responses in whole blood and human monocytes. This anti-inflammatory effect was paralleled by a decreased biosynthesis of arachidonic acid-derived inflammatory LMs, including prostaglandin E2 (PGE2) and thromboxane 2 (TxB2). These findings suggest an anti-inflammatory effect mediated by Lipofermata-mediated redirection of lipid metabolism in monocytes.</div><div>Conversely, in mature human monocyte-derived macrophages, Lipofermata treatment enhanced LPS-induced cytokine production and induced cell death, likely through inflammasome activation. Together, these results underscore the cell type-specific effects of FATP2 inhibition and highlight the dual role of Lipofermata in modulating inflammatory immune responses. As such, targeting lipid metabolism with Lipofermata could have therapeutic potential with both anti- and pro-inflammatory applications, depending on the target cell type and context.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107092"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of islet antigen-specific autoreactive T cells from Japanese patients with slowly progressive insulin-dependent diabetes mellitus","authors":"Noriyuki Kitagawa ,&nbsp;Nobuko Kitagawa ,&nbsp;Ayaka Kobayashi ,&nbsp;Takuro Okamura ,&nbsp;Masahide Hamaguchi ,&nbsp;Michiaki Fukui","doi":"10.1016/j.imlet.2025.107084","DOIUrl":"10.1016/j.imlet.2025.107084","url":null,"abstract":"<div><div>Pancreatic islet antigen-specific autoreactive T cells are involved in inflammation in slowly progressive insulin-dependent diabetes mellitus (SPIDDM). Pancreatic islet antigens, such as glutamic acid decarboxylase 65 (GAD), insulinoma-associated protein 2 (IA-2), and insulin, are associated with SPIDDM. However, the association between pancreatic islet antigen-specific T cells and SPIDDM incidence remains unclear.</div><div>We aimed to identify the characteristics of pancreatic islet antigen autoreactive T cells in Japanese patients with SPIDDM.</div><div>Peripheral blood mononuclear cells were obtained from Japanese patients with type 1 diabetes mellitus (T1DM) enrolled in our diabetic cohort study. An <em>ex vivo</em> cytokine assay using overlapping peptides of GAD, IA-2, and insulin was performed. The production of tumor necrosis factor-alpha (TNF-α) by CD4⁺ T cells and the fractions of TNF-α⁺ CD4⁺ T cell fractions were measured by fluorescence-activated cell sorting.</div><div>The %parent of TNF-α⁺ CD4⁺ T cells and the effector memory TNF-α⁺ CD4⁺ T cells increased after stimulation with overlapping GAD and IA-2 peptides. The response to overlapping peptides was varied among individual SPIDDM case. Response to overlapping peptides of GAD, IA-2, and insulin were observed in each group of T1DM.</div><div>Islet antigen-specific autoreactive TNF-α⁺ CD4⁺ T cells from Japanese patients with SPIDDM were activated by overlapping GAD and IA-2 peptides.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107084"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}