Trypanosoma cruzi infection induces a massive extrafollicular and

BERMEJO D; AMEZCUA VESELY MC; KAHN M; ACOSTA RODRIGUEZ EV; MONTES CL; MERINO C; TOELLNER KM; MOHR E; DALE CUNNINGHAM A; GRUPPI A

IMMUNOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Año: 2011 p. 123 - 133

0019-2805

Acute infection with Trypanosoma cruzi, the etiologic agent of Chagas disease, results in parasitemia and polyclonal lymphocyte activation. It has been reported that polyclonal B cell activation is associated with hypergammaglobulinemia and delayed parasite specific Ab response. In the present study we analyzed the development of B cell response within the different microenvironments of the spleen during acute T. cruzi infection. We observed massive germinal centre (GC) and extrafollicular (EF) responses at the peak of infection. However, the EF foci were evident since day 3 p.i., and, early in the infection, they mainly provided IgM. The EF foci response reached its peak at 11 days p.i. and extended from the red pulp into the PALS. GCs were remarkable since day 8 p.i. At the peak of parasitemia, CD138+ B220+ plasma cells in EF foci, red pulp and T zone expressed IgM and all the IgG isotypes. Instead of the substantial B cell response, most of the Abs produced by splenic cells did not target the parasite, and parasite specific IgG isotypes could be detected in sera only after 18 days p.i. We also observed that the bone marrow of infected mice presented a strong reduction in CD138+ B220+ cells in comparison to normal mice. Then, in acute infection with T. cruzi, the spleen appears as the most important lymphoid organ that lodges plasma cells and the main producer of Abs. The development of B cell response during T. cruzi infection has shown features that are particular to T. cruzi and other protozoan infection but different to other infections or immunization with model Ags.