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,
* Center for Pulmonary and Infectious Disease Control, Departments of
Microbiology and Immunology,
Biochemistry, and
Medicine, University of Texas Health Center, Tyler, TX 75708;
¶ National Cancer Institute, Bethesda, MD 20892; and
|| Epimmune Corp., San Diego, CA 92121
CD8+ T cells play an essential role in immunity to
Chlamydia pneumoniae (Cpn).
However, the target Ags recognized by Cpn-specific
CD8+ T cells have not been identified, and the mechanisms
by which this T cell subset contributes to protection remain unknown.
In this work we demonstrate that Cpn infection primes a
pathogen-specific CD8+ T cell response in mice. Eighteen
H-2b binding peptides representing sequences from 12
Cpn Ags sensitized target cells for MHC class
I-restricted lysis by CD8+ CTL generated from the spleens
and lungs of infected mice. Peptide-specific IFN-
-secreting
CD8+ T cells were present in local and systemic
compartments after primary infection, and these cells expanded after
pathogen re-exposure. CD8+ T cell lines to the 18
Cpn epitope-bearing peptides were cytotoxic, displayed a
memory phenotype, and secreted IFN- and TNF-
, but not IL-4. These
CTL lines lysed Cpn-infected macrophages, and the lytic
activity was inhibited by brefeldin A, indicating endogenous processing
of CTL Ags. Finally, Cpn peptide-specific
CD8+ CTL suppressed chlamydial growth in vitro by direct
lysis of infected cells and by secretion of IFN- and other soluble
factors. These studies provide information on the mechanisms by which
CD8+ CTL protect against Cpn, furnish the
tools to investigate their possible role in immunopathology, and lay
the foundation for future work to develop vaccines against acute and
chronic Cpn infections.
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