Human ImmunologyPub Date : 2025-09-01DOI: 10.1016/j.humimm.2025.111448
E.M. Fore, J. Liu, S. Pandey, T. Harville
{"title":"Virtual crossmatch compatible, with unexpected fluorescence cytometric crossmatch positive, may be safe to proceed with transplantation under certain circumstances","authors":"E.M. Fore, J. Liu, S. Pandey, T. Harville","doi":"10.1016/j.humimm.2025.111448","DOIUrl":"10.1016/j.humimm.2025.111448","url":null,"abstract":"","PeriodicalId":55047,"journal":{"name":"Human Immunology","volume":"86 ","pages":"Article 111448"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145104848","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}
Human ImmunologyPub Date : 2025-09-01DOI: 10.1016/j.humimm.2025.111347
Steven GE. Marsh
{"title":"Nomenclature for factors of the HLA system, update April, May and June 2025","authors":"Steven GE. Marsh","doi":"10.1016/j.humimm.2025.111347","DOIUrl":"10.1016/j.humimm.2025.111347","url":null,"abstract":"","PeriodicalId":55047,"journal":{"name":"Human Immunology","volume":"86 5","pages":"Article 111347"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145265959","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}
Human ImmunologyPub Date : 2025-09-01Epub Date: 2025-08-09DOI: 10.1016/j.humimm.2025.111565
Ping Zhou, Xin Jiang, Wanchun Wang, Dan Wang
{"title":"Dissection of shared genetic architecture and biological association between psoriasis and cardiovascular disease based on genome-wide association studies.","authors":"Ping Zhou, Xin Jiang, Wanchun Wang, Dan Wang","doi":"10.1016/j.humimm.2025.111565","DOIUrl":"10.1016/j.humimm.2025.111565","url":null,"abstract":"<p><strong>Background: </strong>The clinical link between psoriasis (PsO) and cardiovascular diseases (CVDs) is well-established, yet the genetic underpinnings of their comorbidity remain unclear. This study aimed to systematically map the shared genetic architecture between PsO and CVDs to identify key risk loci, effector genes, and biological pathways.</p><p><strong>Methods: </strong>We analyzed large-scale genome-wide association study data for PsO and 11 CVDs to assess their genetic correlation. We then identified pleiotropic loci-variants associated with both PsO and CVDs-and applied colocalization analysis to test whether a single causal variant at each locus could explain the shared association. To interpret these findings, we performed functional annotation to map variants to genes and conducted heritability enrichment analysis to identify critical tissues. Finally, we performed an immune-specific colocalization analysis to investigate the role of distinct immune cell types in driving the shared disease risk.</p><p><strong>Results: </strong>The findings revealed significant shared genetic risk between PsO and seven major CVDs (e.g., hypertension, myocardial infarction, and coronary artery disease). We identified 58 pleiotropic loci at the level of genome-wide significance (P < 5 × 10<sup>-8</sup>). Of these, 11 loci passed causal colocalization tests, indicating a high probability of a shared causal variant. Gene-level analysis pinpointed 97 candidate genes, and through multi-evidence integration, we prioritized four (SLC22A5, LMAN2, HSD3B7, and ZNF668) as high-confidence therapeutic targets. Enrichment analyses showed these shared genes are highly expressed in blood and immune-related tissues and are involved in key pathways such as immune activation and cytokine signaling. Furthermore, our findings suggest that T-cell-mediated immune dysregulation is a key mechanism underlying the comorbidity of PsO and at least five of the studied CVDs.</p><p><strong>Conclusion: </strong>Our systematic genetic analysis identifies shared loci and candidate genes for psoriasis and several cardiovascular diseases. The findings point toward immune-mediated pathways as potential links between these conditions and provide a prioritized list of targets warranting future functional study and therapeutic evaluation.</p>","PeriodicalId":55047,"journal":{"name":"Human Immunology","volume":"86 5","pages":"111565"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144818351","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}
Human ImmunologyPub Date : 2025-09-01DOI: 10.1016/j.humimm.2025.111582
K.P. Sindura , M. Sebastian , P. Davis , L. Srinivas , S. Sathyan , A. Anaswara , M. Padmaja , Moinak Banerjee
{"title":"Proinflammatory phenotype can be critical in defining and modulating the genetic risk of non-syndromic hearing loss","authors":"K.P. Sindura , M. Sebastian , P. Davis , L. Srinivas , S. Sathyan , A. Anaswara , M. Padmaja , Moinak Banerjee","doi":"10.1016/j.humimm.2025.111582","DOIUrl":"10.1016/j.humimm.2025.111582","url":null,"abstract":"<div><div>Non-syndromic hearing loss (NSHL) is a common sensory disorder with a multifactorial origin, involving both genetic and environmental components. Its genetic basis shows significant variability and incomplete penetrance across populations. Environmental factors, especially TORCH infections and sterile inflammation, may contribute to NSHL by triggering inflammatory cascades. Cytokines, secreted proteins crucial in immune regulation, play a central role in mediating these inflammatory responses. This study investigates whether genetic variants in cytokine genes contribute to NSHL susceptibility. A case-control genetic association study was conducted in the Malayalam-speaking Dravidian population, focusing on both pro- and anti-inflammatory cytokine gene variants. The findings reveal, for the first time, a strong association between NSHL and variants in pro-inflammatory cytokines <em>IL1A, IFNG, IL3,</em> and <em>IL12B</em>, along with the anti-inflammatory cytokine <em>IL4</em>. These risk variants were associated with increased pro-inflammatory activity and reduced anti-inflammatory responses. Interactome analysis showed interactions among cytokine genes <em>IL6, IL1B,</em> and <em>TNF</em> with key candidate genes such as <em>GSDME, DIABLO,</em> and <em>GJA1</em>. The results suggest an alternative NSHL pathogenesis mechanism, where environmental influences may act through cytokine gene variants to affect gene expression, possibly via a “Goldilocks effect.” This study underscores the complex interplay of genetic and environmental factors in NSHL development.</div></div>","PeriodicalId":55047,"journal":{"name":"Human Immunology","volume":"86 5","pages":"Article 111582"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144988256","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}