{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fan NW"],"funding":["NEI NIH HHS"],"pagination":["102816"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9106930"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["129"],"pubmed_abstract":["Effector Th17 cells, including IFN-γ<sup>-</sup>IL-17<sup>+</sup> (eTh17) and IFN-γ<sup>+</sup>IL-17<sup>+</sup> (eTh17/1) subsets, play critical pathogenic functions in the induction of autoimmunity. As acute inflammation subsides, a small proportion of the effectors survive and convert to memory Th17 cells (mTh17), which sustain chronic inflammation in autoimmune diseases. Herein, we investigated the differential contributions of eTh17 versus eTh17/1 to the memory pool using an experimental model of ocular autoimmune disease. Our results show that adoptive transfer of Tbx21<sup>-/-</sup> CD4<sup>+</sup> T cells or conditional deletion of Tbx21 in Th17 cells leads to diminished eTh17/1 in acute phase and functionally compromised mTh17 in chronic phase. Further, adoptive transfer of disease-specific eTh17/1, but not eTh17, leads to generation of mTh17 and sustained ocular inflammation. Collectively, our data demonstrate that T-bet-dependent eTh17/1 cells generated during the acute inflammation are the principal effector precursors of pathogenic mTh17 cells that sustain the chronicity of autoimmune inflammation."],"journal":["Journal of autoimmunity"],"pubmed_title":["Autoreactive memory Th17 cells are principally derived from T-bet<sup>+</sup>RORγt<sup>+</sup> Th17/1 effectors."],"pmcid":["PMC9106930"],"funding_grant_id":["P30 EY003790","R01 EY020889"],"pubmed_authors":["Ortiz G","Dana R","Wang S","Fan NW","Chen Y","Chauhan SK"],"additional_accession":[]},"is_claimable":false,"name":"Autoreactive memory Th17 cells are principally derived from T-bet<sup>+</sup>RORγt<sup>+</sup> Th17/1 effectors.","description":"Effector Th17 cells, including IFN-γ<sup>-</sup>IL-17<sup>+</sup> (eTh17) and IFN-γ<sup>+</sup>IL-17<sup>+</sup> (eTh17/1) subsets, play critical pathogenic functions in the induction of autoimmunity. As acute inflammation subsides, a small proportion of the effectors survive and convert to memory Th17 cells (mTh17), which sustain chronic inflammation in autoimmune diseases. Herein, we investigated the differential contributions of eTh17 versus eTh17/1 to the memory pool using an experimental model of ocular autoimmune disease. Our results show that adoptive transfer of Tbx21<sup>-/-</sup> CD4<sup>+</sup> T cells or conditional deletion of Tbx21 in Th17 cells leads to diminished eTh17/1 in acute phase and functionally compromised mTh17 in chronic phase. Further, adoptive transfer of disease-specific eTh17/1, but not eTh17, leads to generation of mTh17 and sustained ocular inflammation. Collectively, our data demonstrate that T-bet-dependent eTh17/1 cells generated during the acute inflammation are the principal effector precursors of pathogenic mTh17 cells that sustain the chronicity of autoimmune inflammation.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-04-19T13:31:09.561Z","creation":"2025-04-19T13:31:09.561Z"},"accession":"S-EPMC9106930","cross_references":{"pubmed":["35395541"],"doi":["10.1016/j.jaut.2022.102816"]}}