We have previously reported that T cells bearing T cell receptors (TCRs) of γ/δ type appear at a relatively early stage of primary infection with Listeria monocytogenes in mice. To characterize the early-appearing γ/δ T cells during listeriosis, we analyzed the specificity and cytokine production of the γ/δ T cells in the peritoneal cavity in mice inoculated intraperitoneally with a sublethal dose of L. monocytogenes. The early-appearing γ/δ T cells, most of which were of CD4− CD8− phenotype, proliferated and secreted IFN-γ 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. To further elucidate the potential role of the 3'//$ T cells in the host-defense mechanism against primary infection with Listeria, we examined the effects of in vivo administration of monoclonal antibodies (mAbs) against TCR-γ/δ or TCR-α/β on the bacterial eradication in mice infected with Listeria. Most of α/β T cells or γ/δ T cells were depleted in the peripheral lymphoid organs at least for 12 d after an intraperitoneal injection of 200/µg TCR-γ/δ mAb or 200 µg TCR-α/β mAb, respectively. An exaggerated bacterial multiplication was evident at the early stage of listerial infection in the γ/δ T cells-depleted mice, whereas the α/β T cell-depleted mice exhibited much the same resistance level as the control mice at this stage although the resistance was severely impaired at the late stage after listerial infection. These results dearly indicated that the early-appearing γ/δ T cells contribute to the host defense at the early stage of infection with Listeria and confirmed previous reports that the highly evolved type of immunity mediated by Listeria-specific α/β T cells contributes to the host protection at the late stage after listerial infection.
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