CD160 serves as a negative regulator of NKT cells in acute hepatic injury

Tae-Jin Kim, Gayoung Park, Jeongmin Kim, Seon Ah Lim, Jiyoung Kim, Kyungtaek Im, Min Hwa Shin, Yang-Xin Fu, Maria-Luisa Rio, Jose-Ignacio Rodriguez-Barbosa, Cassian Yee, Kyung-Suk Suh, Seong-Jin Kim, Sang-Jun Ha () and Kyung-Mi Lee ()
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Tae-Jin Kim: Korea University College of Medicine
Gayoung Park: Korea University College of Medicine
Jeongmin Kim: Korea University College of Medicine
Seon Ah Lim: Korea University College of Medicine
Jiyoung Kim: Korea University College of Medicine
Kyungtaek Im: Korea University College of Medicine
Min Hwa Shin: Korea University College of Medicine
Yang-Xin Fu: University of Texas Southwestern Medical Center
Maria-Luisa Rio: University of Leon
Jose-Ignacio Rodriguez-Barbosa: University of Leon
Cassian Yee: UT MD Anderson Cancer Center
Kyung-Suk Suh: Seoul National University College of Medicine
Seong-Jin Kim: Precision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University
Sang-Jun Ha: Yonsei University
Kyung-Mi Lee: Korea University College of Medicine

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: 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 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.

Date: 2019
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DOI: 10.1038/s41467-019-10320-y

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