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Profound effect of the absence of IL‐4 on T cell responses during infection with Schistosoma mansoni
Author(s) -
PedrasVasconcelos João A.,
Brunet Laura Rosa,
Pearce Edward J.
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.5.737
Subject(s) - biology , schistosoma mansoni , cd8 , immunology , t cell , population , cytotoxic t cell , interleukin 4 , interleukin 2 , cell , interferon gamma , immune system , microbiology and biotechnology , schistosomiasis , helminths , in vitro , demography , sociology , biochemistry , genetics
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)‐γ 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‐γ 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.