Abstract
Gammadelta T cells are unique, and their localization at sites of infection is considered critical in immune defence. We demonstrate the accumulation of gammadelta T cells in rat regional popliteal lymph nodes (PLNi) starting 2 days after inoculation of cytomegalovirus (CMV) into the footpad. Early-appearance PLNi gammadelta T cells significantly inhibited plaque development and the spread of CMV infection. These gammadelta T cells were negative for CD4 and CD8beta receptors, proliferated in response to interleukin-2 (IL-2) and contained high levels of interferon-gamma (IFN-gamma), the appearance of which correlated with the curing of fibroblasts from virus infection. The addition of anti-IFN-gamma abolished the ability of fibroblast monolayers to be cured from CMV infection. In contrast, this protection was not abolished by the addition of anti-rat IL-2 or anti-rat TNF-alpha, or by the depletion of NKR-P1-bearing cells within gammadelta T cells. In addition, the present study shows that while gammadelta T cells derived from naive and CMV-infected rats are able to kill both YAC-1 targets and CMV-infected syngeneic fibroblasts in vitro, only the latter are able to clear CMV-infected fibroblast monolayers. Finally, our data suggest that the expression of NKR-P1 by gammadelta T cells is critical for cytotoxicity, but its contribution to the curing from CMV infection was limited.