SummaryWe have previously reported that T cells bearing T cell receptors (TCRs) of 3`//$ type appear at a relatively early stage of primary infection with Listeria monocytogenes in mice. To characterize the early-appearing 3`//$ T cells during listeriosis, we analyzed the specificity and cytokine production of the 3`//$ T cells in the peritoneal cavity in mice inoculated intraperitoneally with a sublethal dose of L. monocytogenes. The early-appearing 3'//$ T cells, most of which were of CD4-CD8-phenotype, proliferated and secreted IFN-3' and macrophage chemotactic factor in response to purified protein derivative from Mycobacterium tuberculosis, or recombinant 65-kD heat-shock protein derived from M. bov/s but not to heat-killed Listeria.

SUMMARYCytomegalovirus (CMV) causes severe opportunistic infection in immunocompromised hosts. The importance of conventional ab T cells in protection against CMV infection has been well documented. However, the role of the second T-cell population (which express the cd T-cell receptor) in CMV infection is not known. In the present study, we analysed the function and protective role of cd T cells in a murine cytomegalovirus (MCMV) infection model. After intraperitoneal infection with MCMV, the number of cd T cells increased in the liver and peritoneal cavity from day 3, and reached a peak on day 5. The cd T cells showed an activated T-cell phenotype and predominantly expressed Vc1, which is known to be expressed by heat-shock protein 65 (hsp 65)-speci®c cd T cells. Analysis of cytokine expression demonstrated that the MCMV-induced cd T cells expressed interferon-c (IFN-c) and tumour necrosis factor-a (TNF-a) but not interleukin-4 (IL-4), implying their participation in the cell-mediated immune response against MCMV. Depletion of cd T cells by anti-T-cell receptor (TCR) cd monoclonal antibody (mAb) treatment resulted in signi®cant increase of virus titre and decrease of IFN-c in the liver on day 3 after MCMV infection, which further supports the importance of cd T cells in early protection against infection. Finally, the MCMV-induced cd T cells produced IFN-c in vitro in response to hsp 65. Our results suggest that cd T cells participate in early protection against MCMV infection through recognition of hsp 65 and production of IFN-c.

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