@article {1638563,
	title = {Autoreactive memory Th17 cells are principally derived from T-bet+RORγt+ Th17/1 effectors},
	journal = {J Autoimmun},
	volume = {129},
	year = {2022},
	month = {2022 May},
	pages = {102816},
	abstract = {Effector Th17\&nbsp;cells, including IFN-γ-IL-17+ (eTh17) and IFN-γ+IL-17+ (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\&nbsp;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-/- CD4+ T cells or conditional deletion of Tbx21 in Th17\&nbsp;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\&nbsp;cells generated during the acute inflammation are the principal effector precursors of pathogenic mTh17\&nbsp;cells that sustain the chronicity of autoimmune inflammation.},
	keywords = {Autoimmune Diseases, Humans, Inflammation, Interferon-gamma, Interleukin-17, Nuclear Receptor Subfamily 1, Group F, Member 3, Th1 Cells, Th17 Cells},
	issn = {1095-9157},
	doi = {10.1016/j.jaut.2022.102816},
	author = {Fan, Nai-Wen and Wang, Shudan and Ortiz, Gustavo and Chauhan, Sunil K and Chen, Yihe and Dana, Reza}
}
