Abstract
Trypanosoma cruzi infection of mice triggered endogenous production of interleukin-6 (IL-6) during the ascending phase of parasitemia. Injections of anti-IL-6 monoclonal antibody in infected mice at the time of the serum IL-6 peak paradoxically increased IL-6 levels to 60- to 80-fold those in infected mice receiving unrelated immunoglobulins. This early and transient increase in circulating IL-6 levels modified neither the immunoglobulin nor T. cruzi-specific antibody levels of immunoglobulin G1 (IgG1), IgG2a, IgG3, IgM, IgA, and IgE isotypes or the final outcome of infection nor the blood or tissular parasite levels. However, it tended to delay mortality of mice and to increase the levels of the acute-phase protein serum amyloid P component.
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Selected References
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