[초청강연] [2021학년도 1학기 금요세미나] Steady-state memory phenotype cells as bystander T cells to contribute autoimmunity

Steady-state memory phenotype cells as bystander T cells to contribute autoimmunity

Je-Min Choi, Ph.D.
Department of Life Science, College of Natural Sciences, Hanyang University, Korea

T cells generate antigen-specific immune responses to their cognate antigen as a hallmark of adaptive immunity. Despite the importance of antigen-specific T cells, here we show that antigen non-related, innate-like bystander-activated CD4+ T cells are significantly contributing to autoimmune pathogenesis. Single cell RNA sequencing analysis reveals naturally occurring CD44high steady-state memory phenotype cells which contains various effector-like memory clusters such as Th1, Th17, Tfh, Treg, etc. Transcriptome analysis demonstrates that interleukin (IL)-1β- and IL-23-prime T cells that express pathogenic Th17 signature genes such as RORγt, CCR6, and granulocyte macrophage colony-stimulating factor (GM-CSF). Importantly, when co-transferred with myelin-specific 2D2 TCR-transgenic naive T cells to RAGKO mice, unrelated OT-II TCR-transgenic memory-like Th17 cells and/or CCR6high natural memory phenotype cells infiltrate the spinal cord and produce IL-17A, interferon (IFN)-γ, and GM-CSF, increasing the susceptibility of the recipients to experimental autoimmune encephalomyelitis in an IL-1 receptor-dependent manner. In humans, IL-1R1high memory CD4+ T cells are major producers of IL-17A and IFN-γ in response to IL-1β and IL-23. Collectively, our findings reveal the innate-like pathogenic function of antigen non-related steady-state memory CD4 T cells, which contributes to the development of autoimmune diseases.

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