Gamma delta (γδ) T cells play a key role in the innate immune response and serve as the first line of defense against infection and tumors. These cells are defined as tissue-resident lymphocytes in skin, lung, and intestinal mucosa. They are also relatively abundant in the liver; however, little is known about the residency of hepatic γδT cells. By comparing the phenotype of murine γδT cells in liver, spleen, thymus, and small intestine, a CXCR3 + CXCR6 + γδT-cell subset with tissue-resident characteristics was found in liver tissue from embryos through adults. Liver sinusoidal endothelial cells mediated retention of CXCR3 + CXCR6 + γδT cells through the interactions between CXCR3 and CXCR6 and their chemokines. During acute HBV infection, CXCR3 + CXCR6 + γδT cells produced high levels of IFN-γ and adoptive transfer of CXCR3 + CXCR6 + γδT cells into acute HBV-infected TCRδ −/− mice leading to lower HBsAg and HBeAg expression. It is suggested that liver resident CXCR3 + CXCR6 + γδT cells play a protective role during acute HBV infection. Strategies aimed at expanding and activating liver resident CXCR3 + CXCR6 + γδT cells both in vivo or in vitro have great prospects for use in immunotherapy that specifically targets acute HBV infection.
【저자키워드】 liver, Residency, chemotaxis, HBV infection, γδT cells, liver-resident γδT cells,