Intramucosal GPR15-guided regulatory CD8+ T lymphocytes—which are diminished by deleterious GPR15 genetic mutations in severe, early-onset disease or by cell deficiencies in sporadic ulcerat...

Nature - GPR15-guided CD8+ T regulatory cells control intestinal inflammation

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Nature - GPR15-guided CD8+ T regulatory cells control intestinal inflammation

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Read the full paper: Subcellular Redistribution of Endomembrane GPR15 Promotes NAD+-Mediated Metabolic Reprogramming and Boosts 5-FU Chemosensitivity in Colorectal Cancer

Read the full paper: GPR15-GPR15L axis controls colon natural TCRαβ cells residency and enteroendocrine cell homeostasis to calibrate metabolism

Nature Immunology, Published online: 20 August 2026; doi:10.1038/s41590-026-02627-yA population of intramucosal GPR15-guided regulatory CD8+ T cells control intestinal inflammation by inducing cell death in inflammatory macrophages.

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Nature, Published online: 08 June 2026; doi:10.1038/s41586-026-10749-4GPR15-guided CD8+ T regulatory cells control intestinal inflammation

Inflammatory bowel disease (IBD) causes chronic suffering from gastrointestinal inflammation and dysfunction that can progress to colon cancer1,2. The disease prevalence is increasing and there is an urgent need to better understand its pathogenic mechanisms to improve treatment. We show that GPR15, a G protein-coupled receptor (GPCR) expressed in immune cells and previously described as an entry co-factor for human and simian immunodeficiency viruses3, is a marker and homing receptor for a subset of intramucosal GPR15-guided regulatory CD8+ T lymphocytes (CD8+ TIGR). Deleterious GPR15 gene variants in humans cause defective homing of CD8+ TIGR and are associated with severe early-onset IBD. Moreover, CD8+ TIGR cells are reduced in the intestinal mucosa of sporadic IBD patients. In mice, GPR15 deficiency impairs colonic homing of CD8+ TIGR cells, leading to accumulation of inflammatory macrophages and increased susceptibility to colitis. CD8+ TIGR cells potently kill macrophages activated by intestinal damage or disease using Fas ligand (FasL) and TNF-related weak inducer of apoptosis (TWEAK). The identification of CD8+ TIGR cells yields new insights into organ-specific immune regulation and potential therapeutics for IBD...