| First Author | Kim TJ | Year | 2019 |
| Journal | Nat Commun | Volume | 10 |
| Issue | 1 | Pages | 3258 |
| PubMed ID | 31332204 | Mgi Jnum | J:279316 |
| Mgi Id | MGI:6362227 | Doi | 10.1038/s41467-019-10320-y |
| Citation | Kim TJ, et al. (2019) CD160 serves as a negative regulator of NKT cells in acute hepatic injury. Nat Commun 10(1):3258 |
| abstractText | 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-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. |
