We previously reported that γδ T cells appeared and could play a protective role early in infections with intracellular bacteria such as Listeria monocytogenes, Mycobacterium bovis BCG, and Salmonella choleraesuis. To extend these findings to virus infection, we examined the developmental sequence of γδ T cells in bronchoalveolar lavage during the course of Sendai virus infection in C57BL/6 mice. To produce a natural but nonlethal infection course as far as possible, we used a sublethal dose of a wild-type virus which had not been subjected to serial passages in a chicken embryo, hence retaining full virulence for mice. Virus titers in lungs reached a peak on day 6 and then decreased to an undetectable level by day 10. This time course of virus reproduction was immediately and coincidentally followed by the developmental course of γδ T cells, in which the cell number peaked on day 7 and then decreased to a marginal level by day 10. On the other hand, the αβ T-cell number continued to increase until day 10 and remained at a high level thereafter. The early-appearing γδ T cells were CD4-, CD8-, IL-2Rα-β+, CD44+, Mel-14-, and LFA-1α/β+ in phenotype and used Vγ1/2 and Vγ4 and Vδ3, Vδ4, Vδ5, and Vδ6. The γδ T cells were responding to macrophages from infected mice when the cells were cultured in vitro. Furthermore, the expression of endogenous heat shock protein (hsp) was infection specific, and its level appeared to correlate with the γδ T-cell development. These results suggest that the early recruitment of γδ T cells, which proliferate in response to endogeneous hsp+ cells, is also characteristic of this virus infection, although this view appears to be contradictory to earlier reports.
!!!All Science Journal Classification (ASJC) codes