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-Mediated Inhibition
Laboratory of Intracellular Parasites, Immunology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratory, Hamilton, MT 59840
Resistance to the mouse pneumonitis (MoPn) strain of
Chlamydia trachomatis has been mapped to MHC class
II-restricted, IL-12-dependent CD4+ T cells that secrete a
type 1 profile of proinflammatory cytokines, which includes IFN-
and
TNF-
. The relative contribution of IFN- is controversial,
however, due to variation in results presented by different
laboratories. To determine whether C. trachomatis strain
differences contributed to this apparent conflict, the relative
resistance of IFN--deficient mice to murine and human strains of
C. trachomatis was compared. All human serovars were
much more sensitive to the direct inhibitory actions of IFN- than
the MoPn strain. Furthermore, genital clearance of human serovar D in
the C57BL/6 mouse was mediated by class II-independent mechanisms that
probably involved local production of IFN- by cells of the innate
immune system. TNF- also contributed indirectly to host resistance
against all strains tested. The differential susceptibility of distinct
C. trachomatis strains to effector cytokines such as
IFN- could not have been predicted by interstrain biologic variation
or by the profile of cytokines stimulated during infection. These
findings indicate that strain variation should be considered in
situations where related isolates of a given parasite produce
conflicting data in models of infection and immunity. They also suggest
that stimulation of mucosal IFN- activity is a relevant goal for a
human chlamydial vaccine.
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