摘要
NKG2D mediates an important costimulatory pathway in CD8(+) T cells. In HIV infection, the authors found that NKG2D expression on both total CD8(+) and HIV-specific CD8(+) T cells was significantly lower in viremic patients than in HIV controllers. Antiretroviral therapy partially restored NKG2D expression on HIV-specific CD8(+) T cells. The authors observed a negative correlation between the respective expression levels of CD38 and NKG2D on total CD8(+) and HIV-specific CD8(+) T cells. The maintenance of NKG2D expression on CD8(+) T cells in HIV controllers may contribute to better cell function.
- 出版日期2013-1-1