Increased gamma-delta T-lymphocyte response to Mycobacterium bovis BCG in major histocompatibility complex class I-deficient mice

Abstract

Mice with a homologous deletion of the β2-microglobulin gene (β2m-) are deficient in class I major histocompatibility complex molecules (MHC) and consequently are deficient in CD8+ T cells. These β2m-mutant mice control the intraperitoneal growth of an avirulent vaccine strain of mycobacteria, Mycobacterium bovis BCG, after intraperitoneal infection similarly to normal mice. We show that β2m- mice have an increased gamma-delta (γδ) T-cell response after infection with live avirulent mycobacteria. β2m- mice have an earlier and more sustained rise in the proportion of intraperitoneal γδ 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, γδ T cells in the spleens of β2m- mice averaged a higher proportion of the total T-cell population of the spleen on days 5, 8, and 14 after intraperitoneal infection. These data document the kinetics of γδ T cells reactive to mycobacterial antigens in vivo without class I MHC restriction and support a role for class I MHC and CD8+ T cells in the in vivo regulation of γδ T cells.