D. Muller et al., INCREASED GAMMA-DELTA T-LYMPHOCYTE RESPONSE TO MYCOBACTERIUM-BOVIS BCG IN MAJOR HISTOCOMPATIBILITY COMPLEX CLASS I-DEFICIENT MICE, Infection and immunity, 63(6), 1995, pp. 2361-2366
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.