Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY
Correspondence: Dr. Edward J. Pearce, Department of Microbiology and Immunology, C5-165 VMC, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853-6401.
T cell responses of interleukin (IL)-4-/- and wild-type
(WT) mice infected with the helper T cell 2 (Th2) response-inducing
pathogen Schistosoma mansoni were compared. As expected,
given the important role of IL-4 in Th2 response induction, the absence
of IL-4 resulted in diminished Th2 responses, apparent as reduced
production of IL-4, -5, and -10 by CD4+ cells isolated from
the spleens of infected IL-4-/- mice. Surprisingly, these
cells produced significantly less interferon (IFN)-
and proliferated
less than did those from infected WT mice after T cell receptor
ligation. CD8+ cells isolated from infected
IL-4-/- mice also produced less IFN-
than WT CD8
cells, although there was no difference in the proliferative responses
of these cell populations. After infection, spleens of infected
IL-4-/- mice did not enlarge to the same extent as those
of WT mice, and attrition of the CD8+ cell population
within this lymphoid organ was noted. Taken together, the data indicate
that in addition to inhibiting Th2 response development, the lack of
IL-4 during schistosomiasis significantly affects additional aspects of
T cell responses.
Key Words: helminth parasite Th1/Th2 proliferation apoptosis
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