Early appearance of T cell receptor alpha beta + CD4- CD8- T cells with a skewed variable region repertoire after infection with Listeria monocytogenes.

Abstract

We found that the number of T cell receptor (TCR) alpha beta + CD4- CD8- T cells increased in the peritoneal cavity on day 5 after an intraperitoneal infection with Listeria monocytogenes strain EGD together with TCR gamma delta + CD4- CD8- T cells. Thereafter, the TCR alpha beta + CD4- CD8- T cells decreased to a normal level by day 14. The TCR alpha beta + CD4- CD8- T cells showed an activated T cell phenotype (L-selectin CD44 +) and expressed CD45/B220 and interleukin-2 receptor beta, but did not express heat stable antigen, which is expressed by the immature CD4- CD8- thymocytes. Furthermore, 20-30% of the TCR alpha beta + CD4- CD8- T cells expressed the NK1.1 natural killer cell marker. Analysis of the TCR V region repertoire of the TCR alpha beta + CD4- CD8- T cells induced by L. monocytogenes infection showed that more than 80% of the TCR alpha beta + CD4- CD8- T cells expressed TCR V beta 8 detected by anti-TCR V beta 8.1 and 8.2 mAb, and a reverse transcription-polymerase chain reaction analysis of V alpha 14 relative to V alpha 11 expression revealed that the TCR alpha beta + CD4- CD8- T cells expressed a higher level of V alpha 14, which was reported to be preferentially expressed by TCR alpha beta + CD4- CD8- thymocytes rather than conventional CD4+ T cells. The TCR alpha beta + CD4- CD8-T cells showed a proliferative response to anti-TCR alpha beta mAb stimulation. In contrast, they showed no response to stimulation with either Listeria antigen or 65-kDa heat shock protein of Mycobacterium bovis, which do stimulate the Listeria-specific TCR alpha beta + CD4- CD8- T cells and the Listeria-induced TCR gamma delta + T cells, respectively. These results suggest that the TCR alpha beta + CD4- CD8- T cells may recognize a restricted set of self antigens induced by L. monocytogenes infection, and that they contribute to host protection at an early stage of infection.