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CD160 serves as a negative regulator of NKT cells in acute hepatic injury
A research team led by Dr. Kyung-Mi Lee, a professor of Biochemistry and Molecular biology, Korean University College of Medicine, presents a new target for acute hepatitis, which may shed light into the development of a new therapy for liver diseases.
Hepatitis is the main cause of liver diseases. In particular, acute hepatitis causes hepatic cells to die with its strong inflammation, which can further lead to acute liver failure. In acute hepatitis, overly activated immune cells can cause liver injury. Therefore, it is essential to identify the immune cells that are activated during the process along with their mechanism of actions.
CD160 is the receptor expressed on immune cells such as NK cells, NKT cells, and some T cells. It is known to compete BTLA (CD272) in order to bind to the HVEM (CD270) ligand. BTLA, which is expressed on NKT cells had been reported to control excessive immune response by binding to HVEM. So the CD160, which binds to the same ligand of HVEM, was expected to activate NKT cells. Indeed, our team has demonstrated that CD160 functioned as a receptor to activate NK cells (JEM, 2015). However, the currentstudy shows that CD160 is not an NKT cell stimulator but an inhibitor contrary to the expectation. In other words, in acute liver inflammation, there is a rapid increase in the CD160 receptors expressed on NKT cells, which functions like a brake on inflammation.
In the CD160 deficient mice that we produced in order to study the role of CD160 receptor on NKT cells, α-galactosylceramide (α-GalCer) which is NKT cell-specific ligand was applied to see the liver injury speed up and the AST/ALT level increase in the blood. It is also confirmed that the IL-4 and IFN-g cytokine secreted from the NKT ells increased significantly in both cell and animal levels. It is also proven with the Mixed Bone-Marrow Chimera (CD160KO/WT) that the defect is intrinsic to NKT cells. In addition, when acute hepatitis was induced with Concanavalin A (Con A), there was excessive inflammatory response in the CD160 deficient mice, which led to a significant increase in death rate. Findings of our study indicate that the CD160 receptor is a major factor that suppresses overactive immune reaction initiated by NKT cells. This finding is meaningful in that it can contribute to the development of a new therapy of liver disease especially acute hepatitis, targeting the CD160 receptor.
The research results were published in Journal of Nature Communications under the title, CD160 serves as a negative regulator of NKT cells in acute hepatic injury.
pubmed link: https://www.ncbi.nlm.nih.gov/pubmed/31332204
Nat Commun. 2019 Jul 22;10(1):3258. doi: 10.1038/s41467-019-10320-y.