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Interleukin‐4 biases differentiation of B cells from Trypanosoma cruzi ‐infected mice and restrains their fratricide: role of Fas ligand down‐regulation and MHC class II‐transactivator up‐regulation
Author(s) -
Acosta Rodriguez E. V.,
Zuñiga E.,
Montes C. L.,
Gruppi A.
Publication year - 2003
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.0702353
Subject(s) - fas ligand , biology , transactivation , apoptosis , trypanosoma cruzi , microbiology and biotechnology , antibody , immunology , programmed cell death , gene expression , gene , genetics , parasite hosting , world wide web , computer science
In the present work, we demonstrate that interleukin (IL)‐4 is able to rescue B cells from Trypanosoma cruzi ‐infected mice, counteracting the strong apoptotic signals that these cells received in vivo. We have observed that IL‐4 restrains the apoptosis of immunoglobulin (Ig)M + and IgG + B cells from infected and normal mice without inducing them to proliferate. In addition, IL‐4 does not modify the quantity or quality of the antibodies secreted by B cells from infected mice, as it blocks their terminal differentiation to plasma cells and favors memory pathway. It is interesting that the protective effect of IL‐4 over B cells from infected mice is mediated, at least partly, by the down‐regulation of Fas ligand (FasL) expression, which leads to interference in the apoptosis executed by these B cells through the Fas/FasL death pathway. Accordingly, a marked up‐regulation of the “FasL gene repressor” class II transactivator was observed, suggesting that this would be one mechanism underlying the IL‐4‐mediated FasL down‐regulation.