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Trypanosoma cruzi Infection Selectively Renders Parasite-Specific IgG⁺ B Lymphocytes Susceptible to Fas/Fas Ligand-Mediated Fratricide¹

Elina Zuñiga^*, Claudia C. Motran^*, Carolina L. Montes^*, Hideo Yagita and Adriana Gruppi^2,*

^* Department of Clinical Biochemistry, Faculty of Chemical Science, National University of Cordoba, Cordoba, Argentina; and Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan

The control of B cell expansion has been thought to be solely regulated by T lymphocytes. We show in this study that Trypanosoma cruzi infection induces up-regulation of both Fas and Fas ligand (FasL) molecules on B cells and renders them susceptible to B cell-B cell killing (referred to as fratricide throughout this paper) mediated via Fas/FasL. Moreover, by in vivo administration of anti-FasL blocking mAb we demonstrate that Fas-mediated B cell apoptosis is an ongoing process during this parasitic infection. We also provide evidence that B cells that have switched to IgG isotype are the preferential targets of B cell fratricide. More strikingly, this death pathway selectively affects IgG⁺ B cells reactive to parasite but not self Ags. Parasite-specific but not self-reactive B cells triggered during this response are rescued after either in vitro or in vivo FasL blockade. Fratricide among parasite-specific IgG⁺ B lymphocytes could impair the immune control of T. cruzi and possibly other chronic protozoan parasites. Our results raise the possibility that the blockade of Fas/FasL interaction in the B cell compartment of T. cruzi-infected mice may provide a means for enhancing antiparasitic humoral immune response without affecting host tolerance.

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