Piezo1 restrains proinflammatory response but is essential in T-cell-mediated immunopathology.
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ABSTRACT: Piezo1 is a mechanosensitive, nonselective Ca2+ channel that is broadly expressed in CD4+ T cells. Using lineage-specific Piezo1 knockout mice (Piezo1cKO), we show that loss of Piezo1 in CD4+ T cells significantly increased IFNγ and IL-17 production in vitro under TH1 and TH17 polarizing conditions, respectively. Despite their intrinsic proinflammatory phenotype, Piezo1cKO T cells are incapable of establishing disease in vivo in 3 separate adoptive transfer T-cell-mediated inflammatory mouse models, including experimental autoimmune encephalomyelitis, inflammatory bowel disease, and graft-vs-host disease. These phenomena coincided with a decreased effector memory (CD44hiCD62Llo) CD4+ T-cell pool derived from donor Piezo1cKO T cells, an observation related to intrinsic T-cell fitness, as a
SUBMITTER: Choi SH
PROVIDER: S-EPMC11953072 | biostudies-literature | 2025 Mar
REPOSITORIES: biostudies-literature
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