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The Journal of Immunology, Vol 144, Issue 11 4356-4361, Copyright © 1990 by American Association of Immunologists
ARTICLES |
RC Mathew, S Ragheb and DL Boros
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201.
We have previously shown, that anti-L3T4 mAb treatment strongly suppressed granuloma formation in the liver, and IL-2 production in the spleen of Schistosoma mansoni-infected mice. In the present study the dynamics of IL-2 production was delineated during the infection, and the effect of rIL-2 treatment on granulomatous responsiveness was examined. IL-2 production in soluble egg Ag-stimulated spleen cells of mice was detectable at 6, peaked at 8 and waned by 20 wk of the infection. In contrast, Con A stimulus elicited high levels of IL-2 production by 8 wk which remained nearly unchanged throughout the infection. Administration of rIL-2 to acutely infected, anti-L3T4 mAb- treated, or chronically infected mice reversed the diminished or modulated granulomatous responses without restoring the ability for endogenous IL-2 production. Transfer of spleen cells of anti-L3T4 mAb- treated, chronically infected mice did not indicate a role for Ts cells in the impaired production of IL-2 in recipients. These data suggest that lack of IL-2 production can play an important role in the immunoregulation of the granulomatous response.
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