Trypanosoma cruzi infection induces a massive extrafollicular and follicular splenic B cell response which is a high source of non parasite specific antibodies

BERMEJO, DANIELA A; AMEZCUA VESELY, MARIA CAROLINA; KHAN, MAHMOOD; ACOSTA RODRIGUEZ, EVA V; MONTES, CAROLINA L; MERINO, MARIA C; TOELLNER, KM; MOHR, ELODIE; TAYLOR. DALE; CUNNINGHAM, ADAM F; GRUPPI, ADRIANA

WILEY-BLACKWELL PUBLISHING, INC

Lugar: London; Año: 2011 p. 123 - 123

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 11days 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 cel