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, Yet Succumb to Tuberculosis1
*
Department of Molecular Genetics and Biochemistry, and
Central Animal Facilities, University of Pittsburgh School of Medicine, Pittsburgh, PA 15206; and
Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461
CD4 T cells are important in the protective immune response against
tuberculosis. Two mouse models deficient in CD4 T cells were used to
examine the mechanism by which these cells participate in protection
against Mycobacterium tuberculosis challenge. Transgenic
mice deficient in either MHC class II or CD4 molecules demonstrated
increased susceptibility to M. tuberculosis, compared
with wild-type mice. MHC class II-/- mice were more
susceptible than CD4-/- mice, as measured by survival
following M. tuberculosis challenge, but the relative
resistance of CD4-/- mice did not appear to be due to
increased numbers of CD4-8- (double-negative)
T cells. Analysis of in vivo IFN-
production in the lungs of
infected mice revealed that both mutant mouse strains were only
transiently impaired in their ability to produce IFN- following
infection. At 2 wk postinfection, IFN- production, assessed by
RT-PCR and intracellular cytokine staining, in the mutant mice was
reduced by >50% compared with that in wild-type mice. However, by 4
wk postinfection, both mutant and wild-type mice had similar levels of
IFN- mRNA and protein production. In CD4 T cell-deficient mice,
IFN- production was due to CD8 T cells. Thus, the importance of
IFN- production by CD4 T cells appears to be early in infection,
lending support to the hypothesis that early events in M.
tuberculosis infection are crucial determinants of the course
of infection.
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