Influence of the Polyclonal Activation Induced by Plasmodium chabaudi on Ongoing OVA‐Specific B‐ and T‐Cell Responses

Infection by Plasmodium chabaudi results in polyclonal activation, massive proliferation and differentiation of lymphocytes with parasite‐unrelated specificities. To verify if polyclonal activation includes experienced B and T lymphocytes and if it modifies pre‐established cytokine and Ig‐isotype patterns, mice were immunized with ovalbumin (OVA) in alum, a condition that favours T helper 2/immunoglobulin G1 (Th2/IgG1) responses, and infected with P. chabaudi 7 or 80 days later. Polyclonal activation markedly increased the number of anti‐OVA Ig‐secreting cells in the spleen, an effect more patent in mice infected 7 days after OVA immunization, but also evident in mice infected after 80 days. The Ig‐isotype profile predefined by immunization was not qualitatively modified by polyclonal activation. Thus, although P. chabaudi infection preferentially induces IgG2a, the expanded anti‐OVA response is dominated by IgG1. Polyclonal expansion of the anti‐OVA response did not yield an enlarged memory B‐cell pool that could be recalled months later by OVA boosting. Moreover, polyclonal activation of anti‐OVA IgG1‐secreting cells did not increase this antibody in serum, a probable consequence of the high Ig turnover observed during infection. When OVA‐specific T‐cell cytokines were evaluated, we observed an increase of both interleukin‐4 (IL‐4) and interferon‐γ (IFN‐γ) in mice infected 7 days after immunization, whereas in those infected after 80 days, only IL‐4 was augmented. These results suggest that polyclonal activation expands experienced B‐ and T‐cell compartments, preserving their antibody and cytokine patterns.