INCREASED GAMMA-DELTA T-LYMPHOCYTE RESPONSE TO MYCOBACTERIUM-BOVIS BCG IN MAJOR HISTOCOMPATIBILITY COMPLEX CLASS I-DEFICIENT MICE

Mice with a homologous deletion of the beta(2)-microglobulin gene (bet a(2)m(-)) are deficient in class I major histocompatibility complex mo lecules (MHC) and consequently are deficient in CD8(+) T cells. These beta 2m(-) mutant mice control the intraperitoneal growth of an avirul ent vaccine strain of mycobacteria, Mycobacterium bovis BCG, after int raperitoneal infection similarly to normal mice. We show that beta(2)m (-) mice have an increased gamma-delta (gamma delta) T-cell response a fter infection with live avirulent mycobacteria. beta(2)m(-) mice have an earlier and more sustained rise in the proportion of intraperitone al gamma delta T cells, averaging 17% of T cells, compared with 6% in normal mice, at 28 days after infection. Compared with the population in normal mice, gamma delta T cells in the spleens of beta(2)m(-) mice averaged a higher proportion of the total T-cell population of the sp leen on days 5, 8, and 14 after intraperitoneal infection. These data document the kinetics of gamma delta T cells reactive to mycobacterial antigens in vivo without class I MHC restriction and support a role f or class I MHC and CD8(+) T cells in the in vivo regulation of gamma d elta T cells.