{"id":181088,"date":"2026-06-16T08:21:29","date_gmt":"2026-06-16T13:51:29","guid":{"rendered":"https:\/\/newslink360.space\/?p=181088"},"modified":"2026-06-16T08:21:29","modified_gmt":"2026-06-16T13:51:29","slug":"shared-t-cell-signatures-identified-in-ibd","status":"publish","type":"post","link":"https:\/\/newslink360.space\/?p=181088","title":{"rendered":"Shared T Cell Signatures Identified In IBD"},"content":{"rendered":"<p><br \/>\n<\/p>\n<div>\n<p>    <a href=\"https:\/\/www.emjreviews.com\/gastroenterology\/podcasts\/ai-in-ibd\/\" target=\"_blank\" rel=\"noopener\"><span data-contrast=\"none\">IBD<\/span><\/a><span data-contrast=\"auto\">\u00a0linked\u00a0T cell receptor\u00a0(TCR)\u00a0specificity driven by HLA-DRB1 is associated with shared antigen targets and distinct CD4+\u00a0memory T cell signatures across ulcerative colitis and Crohn\u2019s disease. The findings highlight how genetic risk contributes to shaping immune recognition patterns in IBD and may underpin shared inflammatory pathways across disease phenotypes.<\/span><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<h2><b><span data-contrast=\"auto\">HLA-DRB1 Driven T Cell Signatures\u00a0in IBD<\/span><\/b><span data-ccp-props=\"{}\">\u00a0<\/span><\/h2>\n<p><span data-contrast=\"auto\">Researchers genotyped HLA-DRB1 and profiled 3.13 million\u00a0TCR\u00a0beta sequences derived from circulating memory CD4+\u00a0T cells in 33 patients with IBD, including 20 with ulcerative colitis and 13 with Crohn\u2019s disease, alongside 14 healthy controls. Using the GLIPH2 algorithm, 468,441 candidate sequences based on\u00a0CDR3 amino acid motifs were grouped into 440 high confidence\u00a0TCR\u00a0specificity groups. These groups were significantly enriched among individuals sharing HLA-DRB1 alleles,\u00a0indicating\u00a0a strong genetic influence on\u00a0TCR\u00a0specificity in IBD.<\/span><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<h2><b><span data-contrast=\"auto\">Shared Antigen Specificity Groups In IBD<\/span><\/b><span data-ccp-props=\"{}\">\u00a0<\/span><\/h2>\n<p><span data-contrast=\"auto\">Within IBD, five\u00a0TCR\u00a0specificity groups were enriched in patients and shared between ulcerative colitis and Crohn\u2019s disease. This convergence suggests that common antigen targets may contribute to immune activation across different clinical subtypes of IBD, despite variation in affected regions of the gastrointestinal tract. The presence of overlapping specificity groups\u00a0indicates\u00a0that HLA-DRB1 linked selection pressures may shape a unified antigen driven immune response in IBD.<\/span><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<h2><b><span data-contrast=\"auto\">Cytotoxic T Cell Expansion In IBD<\/span><\/b><span data-ccp-props=\"{}\">\u00a0<\/span><\/h2>\n<p><span data-contrast=\"auto\">IBD linked immune profiling also\u00a0demonstrated\u00a0increased frequencies of clonally expanded cytotoxic GZMB+PRF1+\u00a0memory CD4+\u00a0T cells and KIR+\u00a0CD8+\u00a0T cells in a subset of individuals carrying risk alleles. These expansions suggest that specific genetic backgrounds in IBD may promote cytotoxic immune programmes alongside defined\u00a0TCR\u00a0specificity signatures.<\/span><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<p><span data-contrast=\"auto\">Overall, HLA-DRB1 linked\u00a0TCR\u00a0specificity\u00a0provides\u00a0mechanistic insight into how genetic susceptibility shapes antigen recognition and effector T cell activity in IBD. These data support the presence of shared immune pathways across ulcerative colitis and Crohn\u2019s disease and may contribute to future antigen discovery and personalised therapeutic approaches in IBD.<\/span><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<p><b><span data-contrast=\"auto\">Reference<\/span><\/b><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<p><span data-contrast=\"auto\">Chan JE\u00a0et al. Shared CD4+ T cell receptor specificity groups in Crohn\u2019s disease and ulcerative colitis. JCI Insight. 2026; DOI: 10.1172\/jci.insight.195354.\u00a0<\/span><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<p><i><span data-contrast=\"auto\">Featured Image:\u00a0sebra\u00a0on Adobe Stock<\/span><\/i><span data-ccp-props=\"{}\">\u00a0<\/span><\/p>\n<\/div>\n<p><br \/>\n<br \/><a href=\"https:\/\/www.emjreviews.com\/gastroenterology\/news\/shared-t-cell-signatures-identified-in-ibd\/\" target=\"_blank\" rel=\"noopener\">Source link <\/a><\/p>\n","protected":false},"excerpt":{"rendered":"<p>IBD\u00a0linked\u00a0T cell receptor\u00a0(TCR)\u00a0specificity driven by HLA-DRB1 is associated with shared antigen targets and distinct CD4+\u00a0memory T cell signatures across ulcerative colitis and Crohn\u2019s disease. The findings highlight how genetic risk&hellip;<\/p>\n","protected":false},"author":1,"featured_media":181089,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_feature_clip_id":0,"_jetpack_memberships_contains_paid_content":false,"footnotes":"","jetpack_publicize_message":"","jetpack_publicize_feature_enabled":true,"jetpack_social_post_already_shared":true,"jetpack_social_options":{"image_generator_settings":{"template":"highway","default_image_id":0,"font":"","enabled":false},"version":2},"jetpack_post_was_ever_published":false},"categories":[7],"tags":[],"class_list":["post-181088","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-national-news"],"jetpack_publicize_connections":[],"jetpack_featured_media_url":"https:\/\/newslink360.space\/wp-content\/uploads\/2026\/06\/Gastro-12pm-1.jpg","jetpack_likes_enabled":true,"jetpack-related-posts":[{"id":181132,"url":"https:\/\/newslink360.space\/?p=181132","url_meta":{"origin":181088,"position":0},"title":"Heart Failure: A Multisystem Cardiometabolic Disease","author":"Ajay Kumar Verma","date":"June 16, 2026","format":false,"excerpt":"Heart failure (HF) is a clinical syndrome in which structural or functional abnormalities impair cardiac filling or ejection.1 Global prevalence has more than doubled from 25.43 million in 1990 to >64 million people in 2023 and remains a leading cause of hospitalisation in adults aged >65 years. 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