Very large and isotypically atypical polyclonal plaque-forming cell responses in mice infected with Trypanosoma cruzi.

Normal C3H/HeJ mice, acutely infected with T. cruzi, develop large numbers of splenic Ig-secreting plaque-forming cells (PFC). IgG2a, IgG2b and IgG1 PFC account for over 90% of all PFC, while the numbers of IgG3- and IgA-secreting PFC are lower than in normal animals. These effects appear to be due to both T helper-dependent regulation and to a mitogenic activity associated with the parasites themselves.