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.
