The article was published on Nature Medicine in August 2020. Daniele Corridoni et al. (John Radcliffe Hospital, University of Oxford, Oxford, UK) identified colonic CD8+ T-cell phenotypes in health subjects and patients with ulcerative colitis (UC) using single-cell transcriptomics with T-cell receptor repertoire analysis and mass cytometry. Extensive heterogeneity is revealed in CD8+ T-cell composition, including expanded effector and post-effector terminally differentiated CD8+ T cells. In UC, CD8+ effector cells can trigger intestinal damage and secrete tumor necrosis factor (TNF)-α. The innate features of post-effector cells may help these cells adopt regulatory functions that may mitigate excessive inflammation. IL26 induction protects against epithelial damage in a mouse model of acute colitis.
Background & Aims & Conclusions
Colonic antigen-experienced lymphocytes such as tissue-resident memory CD8+ T cells can respond rapidly to repeated antigen exposure.
The phenotypes of colonic antigen-experienced lymphocytes and the mechanisms by which they drive immune regulation and inflammation is still elusive. This study aims at identifying colonic CD8+ T-cell phenotypes in health and UC, defining their clonal relationships, and characterizing terminally differentiated dysfunctional UC CD8+ T cells expressing IL-26.
Extensive heterogeneity is revealed in CD8+ T-cell composition, including expanded effector and post-effector terminally differentiated CD8+ T cells. In UC, CD8+ effector cells can trigger intestinal damage and secrete tumor necrosis factor (TNF)-α. The innate features of post-effector cells may help these cells adopt regulatory functions that may mitigate excessive inflammation. IL26 induction protects against epithelial damage in a mouse model of acute colitis.
