한빛사 논문
Hong-Gyun Lee1,2, Jae-Ung Lee1,2, Do-Hyun Kim1,2, Sangho Lim1,2, Insoo Kang3 & Je-Min Choi1,2,*
1 Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 04763, Republic of Korea. 2 Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Republic of Korea. 3 Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA
*Correspondence and requests for materials should be addressed to J.-M.C.
Abstract
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, bystander memory-like CD4+ T cells also significantly contribute to autoimmune pathogenesis. Transcriptome analysis demonstrates that interleukin (IL)-1β- and IL-23-prime T cells that express pathogenic TΗ17 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, unrelated OT-II TCR-transgenic memory-like TH17 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 memory CD4+ T cells, which contributes to the development of autoimmune diseases.
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