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Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261
The control of acute and chronic Mycobacterium
tuberculosis infection is dependent on CD4+ T
cells. In a variety of systems CD8+ T cell effector
responses are dependent on CD4+ T cell help. The
development of CD8+ T cell-mediated immune responses in the
absence of CD4+ T cells was investigated in a murine model
of acute tuberculosis. In vitro and in vivo, priming of
mycobacteria-specific CD8+ T cells was unaffected by the
absence of CD4+ T cells. Infiltration of CD8+ T
cells into infected lungs of CD4-/- or wild-type mice was
similar. IFN-
production by lung CD8+ T cells in
CD4-/- and wild-type mice was also comparable, suggesting
that emergence of IFN--producing mycobacteria-specific
CD8+ T cells in the lungs was independent of
CD4+ T cell help. In contrast, cytotoxic activity of
CD8+ T cells from lungs of M.
tuberculosis-infected mice was impaired in CD4-/-
mice. Expression of mRNA for IL-2 and IL-15, cytokines critical for the
development of cytotoxic effector cells, was diminished in the lungs of
M. tuberculosis-infected CD4-/- mice. As
tuberculosis is frequently associated with HIV infection and a
subsequent loss of CD4+ T cells, understanding the
interaction between CD4+ and CD8+ T cell
subsets during the immune response to M. tuberculosis is
imperative for the design of successful vaccination
strategies.
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