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(Journal of Leukocyte Biology. 2003;73:127-136.)
© 2003 by Society for Leukocyte Biology

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

E. V. Acosta Rodriguez, E. Zuñiga, C. L. Montes and A. Gruppi

Inmunología, Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas, Universidad Nacional de Cordoba, Argentina

Correspondence: Dr. Adriana Gruppi, Inmunologia, Departamento de Bioquímica Clinica, Facultad de Ciencias Quimicas, Universidad Nacional de Cordoba, Ciudad Universitaria, Haya de la Torre y Medina Allende, Cordoba (5000), Argentina. E-mail: agruppi{at}bioclin.fcq.unc.edu.ar

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.

Key Words: apoptosis • memory B cell • plasma cell • control mechanism • survival




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