CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Role of BAFF in the development of specific and autoreactive humoral response during Trypanosoma cruzi experimental infection
Autor/es:
BERMEJO DA; ACOSTA-RODRÍGUEZ EV; AMEZCUA-VESELY MC; MERINO MC; MONTES CL; GRUPPI A
Lugar:
Rosario, Santa Fé
Reunión:
Congreso; VIII Congreso Argentino de Protozoología y Enfermedades Parasitarias; 2008
Institución organizadora:
Sociedad Argentina de Protozoología
Resumen:
Mice infected with T. cruzi develop splenomegaly showing massive and persistent germinal center and extrafollicular reactions that are accompanied with high levels of parasite-specific and autoreactive Abs. These changes in the spleen B cell compartment coincide with an increase in the amount of BAFF (B cell activating factor belonging to the TNF family), a cytokine involved in peripheral B cell survival and associated to autoimmunity. To analyze the potential role of BAFF in the development of B cell responses during experimental Chagas’ disease, BALB/c mice infected with 500 tripomastigotes were injected i.p. three times/week with 150 ug of BR3:Fc to block BAFF activity, control Ab or PBS, starting at day 1 pi. BAFF blockade decreased the percentage of B cells from spleen and lymph node but not from bone marrow and peritoneum. The reduction in cell numbers was more evident in the mature B cell subset, while the numbers of plasma cells were proportionally increased. Humoral response during T. cruzi infection showed a striking compartmentalization with peritoneum and lymph node cells producing higher amounts of Abs than spleen and bone marrow cells. However, BR3:Fc treated infected mice showed a reduction of total IgM and IgG-isotypes in all the tissues studied. Although it reduced the titers of T. cruzi specific-IgM, BAFF blockade did not affect the titers of parasite-specific IgG or parasitema. In contrast, BAFF blockade was effective to reduce the titers of autoreactive anti-nuclear IgG. Our results suggest that BAFF controls the development of autoreactive IgG as well as parasite-specific IgM responses without targeting parasite replication during T. cruzi infected mice.