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

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

WILEY-BLACKWELL PUBLISHING, INC

Año: 2010 vol. 132 p. 123 - 123

cute infection with Trypanosoma cruzi, the aetiological agent of Chagas' disease, results in parasitaemia and polyclonal lymphocyte activation. It has been reported that polyclonal B-cell activation is associated with hypergammaglobulinaemia and delayed parasite-specific antibody response. In the present study we analysed the development of a 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 post-infection (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 periarteriolar lymphatic sheath. The GCs were detected from day 8 p.i. At the peak of parasitaemia, CD138(+) B220(+) plasma cells in EF foci, red pulp and T-cell zone expressed IgM and all the IgG isotypes. Instead of the substantia