Nature communications · 2019
CD160 serves as a negative regulator of NKT cells in acute hepatic injury.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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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
Аннотация
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 α-galactosylceramide (α-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-γ, TNF, and IL-4 production. Lastly, inhibition of BTLA by anti-BTLA mAb aggravates α-GalCer-induced 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.