EARLY APPEARANCE OF T-CELL RECEPTOR ALPHA-BETA(-) CD8(-) T-CELLS WITHA SKEWED VARIABLE REGION REPERTOIRE AFTER INFECTION WITH LISTERIA-MONOCYTOGENES() CD4()

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 i ntraperitoneal infection with Listeria monocytogenes strain EGD togeth er 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 int erleukin-2 receptor beta, but did not express heat stable antigen, whi ch is expressed by the immature CD4(-)CD8(-) thymocytes. Furthermore, 20-30% of the TCR alpha beta(+) CD4(-) CD8(-) T cells expressed the NK 1.1 natural killer cell marker. Analyses of the TCR V region repertoir e of the TCR alpha beta(+) CD4(-) CD8(-) T cells induced by L. monocyt ogenes infection showed that more than 80% of the TCR alpha beta(+) CD 4(-) 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 reactio n analysis of V alpha 14 relative to V alpha 11 expression revealed th at the TCR alpha beta(+) CD4(-) CD8(-) T cells expressed a higher leve l 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 prolif erative 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 resul ts suggest that the TCR alpha beta(+) CD4(-) CD8(-) T cells may recogn ize a restricted set of self antigens induced by L. monocytogenes infe ction, and that they contribute to host protection at an early stage o f the infection.