Pathogenic function of bystander-activated memory-like CD4+ T cells in autoimmune encephalomyelitisopen access
- Authors
- Lee, Hong-Gyun; Lee, Jae-Ung; Kim, Do-Hyun; Lim, Sangho; Kang, Insoo; Choi, Je-Min
- Issue Date
- Feb-2019
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- NATURE COMMUNICATIONS, v.10, no.1, pp.1 - 14
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURE COMMUNICATIONS
- Volume
- 10
- Number
- 1
- Start Page
- 1
- End Page
- 14
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/15075
- DOI
- 10.1038/s41467-019-08482-w
- ISSN
- 2041-1723
- 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)-1 beta- and IL-23-prime T cells that express pathogenic T(.)17 signature genes such as ROR gamma t, 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 T(H)17 cells infiltrate the spinal cord and produce IL-17A, interferon (IFN)-gamma, and GM-CSF, increasing the susceptibility of the recipients to experimental autoimmune encephalomyelitis in an IL-1 receptor-dependent manner. In humans, IL-1R1(high) memory CD4(+) T cells are major producers of IL-17A and IFN-gamma in response to IL-1 beta 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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