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Infection and Immunity, March 1999, p. 1379-1385, Vol. 67, No. 3
0019-9567/99
Clearance of Chlamydia trachomatis from
the Murine Genital Mucosa Does Not Require Perforin-Mediated
Cytolysis or Fas-Mediated Apoptosis
Linda L.
Perry,
Karen
Feilzer,
Scott
Hughes, and
Harlan D.
Caldwell*
Laboratory of Intracellular Parasites, Rocky
Mountain Laboratories, National Institute of Allergy and Infectious
Diseases, National Institutes of Health, Hamilton, Montana 59840
Received 20 October 1998/Returned for modification 25 November
1998/Accepted 15 December 1998
The molecular mechanisms of resistance to genital infection with
the mouse pneumonitis (MoPn) strain of Chlamydia
trachomatis are unknown. A role for major histocompatibility
complex class II-restricted, interleukin-12-dependent CD4+
T cells has been established, but the functional activity of these
cells does not depend on secretion of gamma interferon. Here we
examined the potential contribution of T-cell-mediated cytotoxicity and
apoptosis to mucosal clearance of MoPn by using mice deficient in the
molecular mediators of target cell lysis. Animals lacking perforin,
Fas, Fas ligand, or both perforin and Fas ligand were infected
genitally with C. trachomatis MoPn and monitored for
expression of immunity to chlamydial antigens and clearance of MoPn
from the genital mucosa. In each case, the profile of spleen cytokine
production, the magnitude of the host antibody response, and the
kinetics of chlamydial clearance were similar to those of genetically
intact controls. Compensatory overproduction of tumor necrosis factor
alpha, an alternate mediator of apoptosis in certain cell types, did
not appear to account for the ability of mutant mice to resolve
Chlamydia infections. These results fail to support
CD4+ T-cell-mediated apoptosis or CD8+
T-cell-mediated cytotoxicity as being critical to the clearance of
C. trachomatis MoPn urogenital infections.
*
Corresponding author. Mailing address: Laboratory of
Intracellular Parasites, Rocky Mountain Laboratories, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health, 903 S. 4th St., Hamilton, MT 59840. Phone: (406) 363-9333. Fax: (406) 363-9355. E-mail: harlan_caldwell{at}nih.gov.
Infection and Immunity, March 1999, p. 1379-1385, Vol. 67, No. 3
0019-9567/99
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