Immunological Investigations最新文献

{"title":"Rewiring Food Allergy Management: From Allergen Detection to Immune Engineering Therapies.","authors":"Jiaqi Meng, Leyan Zhao, Qinglin Wei, Pengcheng Wei","doi":"10.1080/08820139.2026.2746691","DOIUrl":"https://doi.org/10.1080/08820139.2026.2746691","url":null,"abstract":"<p><strong>Background: </strong>Food allergy represents a growing global health challenge, particularly among children in developed countries. Despite decades of research, major barriers persist in both allergen detection and durable immune intervention.</p><p><strong>Methods: </strong>This review synthesizes current diagnostic and therapeutic strategies in food allergy, critically evaluates their mechanistic underpinnings and translational readiness.</p><p><strong>Results: </strong>Traditional immunoassays (e.g. enzyme-linked immunosorbent assay, immunoblotting) are sensitive but hindered by matrix interference, operational complexity, and limited real-world applicability. Recent innovations - multi-omics, DNA-based platforms, and portable biosensors - are advancing allergen surveillance toward precision, on-site detection. In parallel, allergen-specific immunotherapies have emerged as proactive strategies for desensitization, yet vary in efficacy, safety, and sustainability. Biologics (e.g. omalizumab, dupilumab) have broadened treatment options, while next-generation platforms - virus-like particle vaccines and microbiome-augmented protocols - are unlocking novel paths toward sustained unresponsiveness.</p><p><strong>Conclusions: </strong>This review outlines an emerging framework of immune engineering poised to redefine the future of allergy care.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-23"},"PeriodicalIF":2.3,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181593","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":"Metabolic-Epigenetic Reprogramming of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis: Perspectives for Traditional Chinese Medicine.","authors":"Jinling Zhang, Ke Han","doi":"10.1080/08820139.2026.2747770","DOIUrl":"https://doi.org/10.1080/08820139.2026.2747770","url":null,"abstract":"<p><strong>Background: </strong>In rheumatoid arthritis (RA), persistent synovial inflammation and clinical relapse cannot be fully explained by immune activation alone, as fibroblast-like synoviocytes (FLS) can acquire stable pathogenic states that sustain synovitis and joint destruction. Metabolic reprogramming and epigenetic remodeling are functionally integrated in RA-FLS, thereby promoting hyperproliferation, invasiveness, apoptosis resistance, and inflammatory memory.</p><p><strong>Methods and results: </strong>In this review, we summarize the interplay between altered cellular metabolism and epigeneticmechanisms, including DNA methylation, histone modifications, non-coding RNAs, RNA modifications, and chromatin remodeling, and discuss how this interplay contributes tostabilizing pathogenic FLS phenotypes.We further discuss gut microbiota-associated metabolites, including short-chain fatty acids, bile acids, tryptophan derivatives, and one-carbon metabolites, as potential mediators linking systemic metabolic imbalance to FLS epigenetic states. These metabolites may act through histone deacetylase (HDAC) inhibition, modulation of methyl donor availability, and receptor-mediated inflammatory signaling. From the perspective of Traditional Chinese Medicine (TCM), we propose that TCM formulations and bioactive compounds may modulate this network through microbiota-dependent metabolic remodeling and direct suppression of FLS activation. Finally, we identify current evidence gaps and highlight emerging therapeutic strategies, including metabolomics-guided fecal microbiota transplantation and FLS-targeted epigenetic interventions.</p><p><strong>Conclusion: </strong>This review highlights metabolic-epigenetic reprogramming as a key mechanism underlying persistent RA-FLS phenotypes. Interactions among thegut microbiota, microbial metabolites, and epigenetic regulation provide a promising framework for linking systemic metabolic disturbances to local joint damage. Future studies integrating multi-omics profiling, microbiome modulation, and FLS-targeted epigenetic interventions are needed to clarify causality and facilitate more precise therapeutic strategies.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-47"},"PeriodicalIF":2.3,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181576","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":"Decoding the IL-12 Cytokine Family in Sjögren's Disease: Pathogenic Networks and Translational Implications.","authors":"Manyu Han, Jiaqi Yang, Feng Gao, Xing Sui","doi":"10.1080/08820139.2026.2742254","DOIUrl":"https://doi.org/10.1080/08820139.2026.2742254","url":null,"abstract":"<p><strong>Background: </strong>Sjögren's disease (SjD) is a systemic autoimmune disorder characterized by exocrine-gland dysfunction and heterogeneous extraglandular manifestations. The IL-12 cytokine family, comprising IL-12, IL-23, IL-27, and IL-35, may contribute to SjD through interconnected immune and JAK-STAT signaling pathways.</p><p><strong>Objective: </strong>To review the roles of IL-12-family cytokines in SjD pathogenesis and identify current knowledge gaps and translational challenges.Methods: A narrative literature search was conducted using PubMed/MEDLINE, Scopus, and Web of Science. Keywords and combinations related to SjD, IL-12, IL-23, IL-27, IL-35, cytokine signaling, JAK-STAT pathways, and immune responses were used to identify relevant studies. Human and experimental studies addressing the biological or pathological roles of IL-12-family cytokines in SjD were considered, and reference lists of relevant publications were additionally screened.</p><p><strong>Results: </strong>IL-12 promotes STAT4-dependent Th1 differentiation and IFN-γ production, whereas IL-23 supports pathogenic Th17 responses. IL-27 exhibits context-dependent regulatory or proinflammatory effects, while IL-35 is generally associated with immunoregulatory activity, although human findings remain inconsistent.</p><p><strong>Conclusion: </strong>IL-12-family cytokines may function as an interconnected network in SjD rather than independently. Further longitudinal and tissue-specific studies are needed to validate their potential for patient stratification and therapeutic targeting.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-32"},"PeriodicalIF":2.3,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136415","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":"Investigation of Wnt2's Role in Macrophage Polarization and Its Effects on Sepsis.","authors":"Yanfang He, Jianfen Sun, Wenkai Xiao, Qiu Huang, Yao Lin, Jing Tang","doi":"10.1080/08820139.2026.2712497","DOIUrl":"https://doi.org/10.1080/08820139.2026.2712497","url":null,"abstract":"<p><strong>Objective: </strong>Sepsis, characterized by organ dysfunction from an uncontrolled immune response to infection, remains a leading cause of mortality in critical care settings. A key underlying mechanism involves the imbalance between pro-inflammatory M1-type macrophages and anti-inflammatory M2-type macrophages in the biphasic pathological process of 'cytokine storm-immunosuppression' in sepsis. These macrophages, as crucial effector cells of innate immunity, contribute to multi-organ injury.</p><p><strong>Methods: </strong>This article presents a comprehensive review of a large body of relevant literature. Wnt2, a secreted glycoprotein from the Wnt signaling family, performs distinct immunomodulatory roles. The classic Wnt/β-catenin signaling pathway interacts with key regulatory nodes like NF-κB and metabolic reprogramming to regulate macrophage phenotype switching, balance inflammatory cytokine release, and protect organs including the lungs, intestines, heart, and liver during sepsis.</p><p><strong>Results: </strong>This article provides a comprehensive overview of the molecular characteristics of Wnt2, the pathological significance of macrophage polarization in sepsis, the molecular network underlying Wnt2-mediated macrophage polarization and inflammatory regulation, and the prospects for clinical translation.</p><p><strong>Conclusions: </strong>The study establishes an integrative framework linking 'Wnt/β-catenin-macrophage polarization-sepsis,' providing a theoretical basis for the development of targeted immunotherapeutic strategies for sepsis.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-13"},"PeriodicalIF":2.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109061","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":"Childhood-Onset Systemic Lupus Erythematosus: Genetic Mechanisms and Therapeutic Strategies.","authors":"Yuxing Shi, Zaiquan Shi, Lifang Zhang, Yiming Tong, Weiqun Bao, Xulai Shi","doi":"10.1080/08820139.2026.2738417","DOIUrl":"https://doi.org/10.1080/08820139.2026.2738417","url":null,"abstract":"<p><strong>Objective: </strong>Childhood-onset systemic lupus erythematosus (cSLE) is more aggressive than adult SLE, with higher rates of lupus nephritis, organ damage, and early mortality. This review synthesizes recent advances in cSLE genetics and targeted therapies.</p><p><strong>Methods: </strong>We conducted a comprehensive literature search in PubMed and Web of Science using keywords including \"childhood-onset SLE,\" \"monogenic lupus,\" \"type I interferon,\" \"targeted therapy,\" \"JAK inhibitors,\" and \"CAR-NK.\" We prioritized high-quality original research, systematic reviews, randomized controlled trials, and landmark case reports.</p><p><strong>Results: </strong>High-throughput sequencing has identified monogenic variants in 3.5-15% of cSLE patients, predominantly in complement, type I interferon, and immune tolerance genes. Single-cell and spatial transcriptomics have established type I interferon overactivation as a central driver, revealed age-specific B-cell defects, and uncovered early molecular alterations in the kidney microenvironment. Therapeutically, belimumab, telitacicept, anifrolumab, JAK inhibitors, rituximab and emerging CAR-NK therapy are shifting treatment toward precision targeting, with genotype-guided therapy showing notable success in monogenic lupus.</p><p><strong>Conclusion: </strong>Major challenges persist, including scarce pediatric-specific trials, delayed translation of genetic findings, heterogeneous treatment responses, and unknown long-term safety. Addressing these gaps through multicenter cohorts, pediatric-specific randomized controlled trials, and biomarker-driven algorithms will transform cSLE management from adult-data extrapolation to molecular subtyping and tailored therapy.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-27"},"PeriodicalIF":2.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109089","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":"Blockade of the PD-1 / PD-L1 Axis Exacerbates Chronic <i>Nocardia Brasiliensis</i> Infection by Disrupting Bacterial Immune Containment in BALB/c Mice.","authors":"Maria L Ruiz-de la Cruz, Anna V Vazquez-Marmolejo, Manuel G Mejia-Torres, Maria A Castro-Corona, Mario C Salinas-Carmona","doi":"10.1080/08820139.2026.2731121","DOIUrl":"https://doi.org/10.1080/08820139.2026.2731121","url":null,"abstract":"<p><strong>Background: </strong>Therapeutic blockade of the PD-1/PD-L1 axis is a key strategy in cancer immunotherapy to reverse T cell exhaustion. However, this approach carries the risk of reactivating latent pathogens in individuals with chronic infections. The role of this immune checkpoint in granulomatous infectious diseases, particularly chronic actinomycetoma, remains largely unexplored.</p><p><strong>Methods: </strong>To investigate this, we treated BALB/c mice with established chronic <i>Nocardia brasiliensis</i> actinomycetoma using the PD-L1 inhibitor atezolizumab. We assessed survival, clinical progression, and histopathology, and characterized systemic versus local immune responses through cytokine analysis and flow cytometry of lymphoid organs and lesion tissue.</p><p><strong>Results: </strong>Actinomycetoma lesions had a paucicellular lymphocyte infiltrate, yet the few CD8+ T cells present exhibited high PD-1 expression. Atezolizumab treatment was associated with increased mortality, loss of granuloma integrity, exacerbated necrosis, and higher bacterial load in survivors, although the precise cause of death was not directly established. These outcomes occurred despite the absence of classical clinical signs of sepsis and elevations in hallmark proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). PD-L1 blockade triggered a paradoxical cytokine profile (elevated IL-12p70 and IL-10) but failed to reprogram the neutrophil-dominated microenvironment.</p><p><strong>Conclusion: </strong>These findings provide evidence that PD-1/PD-L1 signaling is associated with the maintenance of immune equilibrium and bacterial containment in chronic <i>N. brasiliensis</i> infection in our murine model. Although the absence of an isotype control remains a methodological limitation, anti-PD-L1 therapy was accompanied by severe immunopathology and reduced survival, highlighting potential risks of checkpoint inhibitors during underlying chronic infections.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-27"},"PeriodicalIF":2.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016562","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":"Attenuation of Neutrophil Extracellular Trap Formation in Lipopolysaccharide-Induced Acute Lung Injury Associated with Cinnamaldehyde.","authors":"Nian Cao, Yue Dai, Juan Feng, Xinyun Xu, Jianqiang Xu","doi":"10.1080/08820139.2026.2729077","DOIUrl":"https://doi.org/10.1080/08820139.2026.2729077","url":null,"abstract":"<p><strong>Background: </strong>Excessive neutrophil activation and neutrophil extracellular trap (NET) formation play critical roles in the pathogenesis of acute lung injury (ALI). Cinnamaldehyde, a major bioactive component of cinnamon, has been reported to exert anti-inflammatory effects; however, its impact on NET formation in ALI remains unclear.</p><p><strong>Methods: </strong>A lipopolysaccharide (LPS)-induced ALI rat model and a PMA-stimulated primary neutrophil model were employed to evaluate the effects of cinnamaldehyde in vivo and in vitro. Lung injury severity, pulmonary edema, inflammatory cell infiltration, cytokine production, and NET-associated markers were assessed using histopathology, wet-to-dry ratio analysis, BALF examination, immunofluorescence staining, and Western blotting.</p><p><strong>Results: </strong>Cinnamaldehyde significantly alleviated LPS-induced lung injury, as evidenced by reduced lung wet-to-dry ratios and improved histopathological scores compared with the LPS group (<i>p</i> < .001). Treatment with cinnamaldehyde markedly decreased inflammatory cell and neutrophil infiltration in BALF and suppressed TNF-α, IL-6, and MCP-1 levels (<i>p</i> < .05-0.001). Furthermore, cinnamaldehyde significantly inhibited NET formation in lung tissues, as indicated by reduced levels of myeloperoxidase, cell-free DNA, citrullinated histone H3, and neutrophil elastase (<i>p</i> < .001). In vitro, cinnamaldehyde directly suppressed PMA-induced NET release from primary neutrophils without affecting cell viability (<i>p</i> < .001).</p><p><strong>Conclusion: </strong>These findings demonstrate that cinnamaldehyde protects against LPS-induced acute lung injury by suppressing excessive NET formation, highlighting NET inhibition as a key mechanism underlying its pulmonary protective effects.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-16"},"PeriodicalIF":2.3,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989844","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":"Vitamin D Receptor <i>BsmI</i> Polymorphism and Inflammatory Features in Juvenile Idiopathic Arthritis.","authors":"Rasha M Abdel-Hamid, Amal Ahmed Mohamed, Mohamed Abdel-Megid, Omnia A M Abd El-Ghafar, Sherin A Taha, Dina A Mohareb, Mohamed Abdelfattah Ibrahim Saad, Omnia M Anwer, Shaimaa Emad El Abrak, Eman AlHussain A Gawad, May Selim, Abbas Mohamed Abbas, Mohamed Mamdouh Sherif, Wessam Ali Al-Kholy, Mohammed A Alqaad, Rasha Aguib Hassan Ali","doi":"10.1080/08820139.2026.2729084","DOIUrl":"10.1080/08820139.2026.2729084","url":null,"abstract":"<p><strong>Background: </strong>Vitamin D and vitamin D receptor (VDR) gene polymorphisms influence immune regulation, but their role in juvenile idiopathic arthritis (JIA) remains unclear. We aimed to examine the association between BsmI VDR gene polymorphism and JIA susceptibility in children and evaluate its relationship with inflammatory biomarkers.</p><p><strong>Methods: </strong>Sixty-nine children with JIA and 69 healthy controls were enrolled over two years. Serum vitamin D levels were analyzed using the calcidiol 25-hydroxyvitamin D (25(OH)D) enzyme-linked immunosorbent assay (ELISA). Participants' biochemical and inflammatory markers, hematological parameters, demographics, medical histories, and dietary patterns were also assessed. Genotyping of the <i>BsmI</i> VDR gene polymorphism (rs1544410) was done using real-time polymerase chain reaction (PCR).</p><p><strong>Results: </strong>Interleukin-6 (IL-6), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were significantly higher in patients with JIA (<i>p</i> = 0.001, < 0.001, and < 0.001, respectively). The <i>BsmI</i> AA genotype was significantly associated with JIA (<i>p</i> < 0.001). Multivariate analysis revealed that the rs1544410 <i>VDR</i> gene polymorphism (AA versus GG) and age were independent factors associated with JIA (OR 8.404, 95% CI 2.835-24.913, <i>p</i> < 0.001; OR 1.325, 95% CI 1.063-1.653, <i>p</i> = 0.012, respectively). No significant differences were observed in inflammatory markers, tumor necrosis factor-alpha (TNF-α), IL-6, ESR, and CRP, among VDR genotypes (all <i>p</i> > 0.05).</p><p><strong>Conclusion: </strong>The <i>BsmI</i> (rs1544410) VDR gene polymorphism is significantly associated with susceptibility to JIA, with the AA genotype as an independent predictor. However, no significant relationship was observed between genotypes and inflammatory biomarkers, suggesting that this polymorphism may contribute to disease susceptibility rather than modulating inflammatory activity.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-15"},"PeriodicalIF":2.3,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982629","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":"Therapeutic Cancer Vaccines: Classification, Mechanisms, Challenges and Future Perspectives.","authors":"Juwei Gao, Yue Sun, Zijing Han, Huiwen Zhang, Mingwei Sun, Shujun Liu, Bo Zhang","doi":"10.1080/08820139.2026.2733761","DOIUrl":"https://doi.org/10.1080/08820139.2026.2733761","url":null,"abstract":"<p><strong>Background: </strong>With the rapid advancements in oncology, immunology, and molecular biology, immunotherapy has emerged as a cornerstone of anti-tumor treatment, complementing traditional modalities such as surgery, radiotherapy, and chemotherapy. Therapeutic cancer vaccines are a promising immunotherapy strategy that deliver tumor-associated antigens or neoantigens to prime naive T cells and generate long-lived memory cells for durable anti-tumor immunity. Recent advances in neoantigen identification, mRNA technology, biomaterial delivery and combination immunotherapy accelerate the development of personalized cancer vaccines. However, their clinical efficacy remains suboptimal, limited by poor immunogenicity, tumor heterogeneity, immune escape and immunosuppressive TME.</p><p><strong>Objectives: </strong>This review classifies therapeutic cancer vaccines by antigen source and design strategy, analyzes key biological barriers limiting efficacy, summarizes clinical trial evidence, and discusses strategies to overcome these bottlenecks.</p><p><strong>Methods: </strong>We systematically reviewed published literature regarding cancer vaccine design, delivery platforms, clinical trials and combination immunotherapy.</p><p><strong>Results: </strong>Multiple biological obstacles restrict vaccine efficacy. Novel approaches including computational antigen design, advanced RNA platforms, optimized delivery, biomarker-guided vaccination and rational combination therapy can mitigate these barriers.</p><p><strong>Conclusions: </strong>These advances provide an integrated framework for developing next-generation therapeutic cancer vaccines and advancing precision cancer immunotherapy.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-35"},"PeriodicalIF":2.3,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976669","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":"<i>MSH5</i> Gene Polymorphisms Are Associated with Hashimoto's Thyroiditis Susceptibility in a Chinese Han Population.","authors":"Xinwei Zhang, Yanfei Jiang, Wenyu Xu, Guangxin Li, Yalin Wang, Qiu Qin, Na Li, Jin-An Zhang","doi":"10.1080/08820139.2026.2729081","DOIUrl":"https://doi.org/10.1080/08820139.2026.2729081","url":null,"abstract":"<p><strong>Background: </strong>This study investigated associations between <i>MSH5</i> polymorphisms and autoimmune thyroid disease (AITD) susceptibility.</p><p><strong>Methods: </strong>We genotyped rs409558 and rs707939 in 943 patients with AITD, including 591 with Graves' disease (GD) and 352 with Hashimoto's thyroiditis (HT), and 488 controls. Genetic associations were assessed before and after adjustment for age and sex. MAX3 testing with Bonferroni correction and haplotype analysis were performed. Linkage disequilibrium was assessed in healthy controls.</p><p><strong>Results: </strong>rs409558 was not associated with AITD or its subtypes. The unadjusted association between rs707939 and overall AITD was attenuated after adjustment. Associations with HT remained significant after adjustment (allele model: OR = 1.28, <i>p</i> = .032; dominant model: OR = 1.84, <i>p</i> = .016). MAX3 testing favored the additive model for HT, with significance retained after Bonferroni correction. The variants shared a haplotype block, with high D' (0.96) but low r² (0.10), indicating limited allelic correlation. The TA haplotype was associated with reduced HT risk (OR = 0.64, 95% CI: 0.51-0.81, <i>p</i> < .001).</p><p><strong>Conclusion: </strong><i>MSH5</i> rs707939 and the TA haplotype were associated with HT susceptibility. Further studies are needed to validate these associations and clarify their functional basis.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-16"},"PeriodicalIF":2.3,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962899","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}