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Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada
T cell-mediated immunity as measured by delayed-type
hypersensitivity, and IFN-
production has been shown to be critical
for host defense against Chlamydia trachomatis infection
in both human and animal studies. Using gene-targeted B cell-deficient
mice, we examined the role of B cells in protective immunity to
C. trachomatis (mouse pneumonitis) (MoPn) lung
infection. B cell-deficient mice were observed to have a significantly
higher mortality rate and in vivo chlamydial growth than did wild-type
mice following MoPn lung infection. Interestingly, B cell-deficient
mice not only lacked Ab responses but also failed to mount an efficient
delayed-type hypersensitivity response following chlamydial lung
infection. In contrast to results obtained from MoPn-infected wild-type
C57BL/6 mice, spleen cells from infected B cell-deficient mice failed
to produce Th1-related (IFN-) or Th2-related (IL-6 and IL-10)
cytokines after Chlamydia-specific in vitro
restimulation. Moreover, unlike wild-type mice, B cell-deficient mice
were not immune to rechallenge infection following recovery from
primary chlamydial infection. The data indicate that B cells play an
important role in host defense to primary and secondary chlamydial
infection and suggest that B cells are crucial for the initiation of
early T cell responses to chlamydial infection. This study provides
evidence for the role of B cells in the in vivo priming of T cells
during infection with the intracellular bacterial pathogen, C.
trachomatis.
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