CD160 serves as a negative regulator of NKT cells in acute hepatic injury
- Authors
- Kim, Tae-Jin; Park, Gayoung; Kim, Jeongmin; Lim, Seon Ah; Kim, Jiyoung; Im, Kyungtaek; Shin, Min Hwa; Fu, Yang-Xin; Del Rio, Maria-Luisa; Rodriguez-Barbosa, Jose-Ignacio; Yee, Cassian; Suh, Kyung-Suk; Kim, Seong-Jin; Ha, Sang-Jun; Lee, Kyung-Mi
- Issue Date
- 22-7월-2019
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- NATURE COMMUNICATIONS, v.10
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURE COMMUNICATIONS
- Volume
- 10
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/64076
- DOI
- 10.1038/s41467-019-10320-y
- ISSN
- 2041-1723
- Abstract
- CD160 and BTLA both bind to herpes virus entry mediator. Although a negative regulatory function of BTLA in natural killer T (NKT) cell activation has been reported, whether CD160 is also involved is unclear. By analyzing CD160(-/-) mice and mixed bone marrow chimeras, we show that CD160 is not essential for NKT cell development. However, CD160(-/-) mice exhibit severe liver injury after in vivo challenge with alpha-galactosylceramide (alpha-GalCer). Moreover, CD160(-/-) mice are more susceptible to Concanavalin A challenge, and display elevated serum AST and ALT levels, hyperactivation of NKT cells, and enhanced IFN-gamma, TNF, and IL-4 production. Lastly, inhibition of BTLA by anti-BTLA mAb aggravates alpha-GalCerinduced hepatic injury in CD160(-/-) mice, suggesting that both CD160 and BTLA serve as non-overlapping negative regulators of NKT cells. Our data thus implicate CD160 as a co-inhibitory receptor that delivers antigen-dependent signals in NKT cells to dampen cytokine production during early innate immune activation.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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