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J. Exp. Med.,
Volume 189, Number 12, June 21, 1999 1973-1980
By
From the * Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and
Harvard Medical School, Boston, Massachusetts 02115; the Cellular immunity against Mycobacterium tuberculosis controls infection in the majority of infected humans. Studies in mice have delineated an important role for CD4+ T cells and cytokines including interferon Department of Immunology and
Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115; and the § Gwen
Knapp Center for Lupus and Immunology Research, University of Chicago, Chicago, Illinois 60637
and tumor necrosis factor 
in the response to infection with mycobacteria. Recently, the identification of CD8+ CD1-restricted T cells that kill M. tuberculosis
organisms via granulysin and the rapid death after infection of 
2 microglobulin deficient mice
in humans has drawn attention to a critical role for CD8+ T cells. The nature of mycobacterial-specific CD8+ T cells has been an enigma because few have been identified in any species.
Here, we delineate the contribution of class I MHC-restricted T cells in the defense against tuberculosis as transporter associated with antigen processing (TAP)1-deficient mice died rapidly, bore a greater bacterial burden, and had more severe tissue pathology than control mice. In contrast,
CD1D
/ mice were not significantly different in their susceptibility to infection than control
mice. This data demonstrates a critical role for TAP-dependent peptide antigen presentation and
provides further evidence that class I MHC-restricted CD8+ T cells, the major T cell subset
activated by this antigen processing pathway, play an essential role in immunity to tuberculosis.
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