Abstract

Leishmaniasis presents a complex spectrum of diseases and immunological manifestations depending upon both the species of the microorganism and the host it infects. BALB/c mice, which are homozygous for Lsh(s) on chromosome 1, are genetically susceptible to the visceralizing species of Leishmania. Infection of these mice with an Indian strain of Leishmania donovani showed a steady rise in the level of parasite burden in both the liver and the spleen to 24 wk. To investigate the immune responses determining the course of infection, we studied the relative levels of specific IgG, IgM, and IgA antibodies, and IgG isotypes, in the sera of diseased and protectively immunized mice at different periods of infection. IgG1 and IgG2a were stimulated in the control, infected, and immunized mice after parasite challenge. However, an early induction of IgG1 in the normal infected mice and stimulation of IgG2a and IgG2b isotypes prior to parasite challenge in liposome-antigen-immunized mice suggest that the elicitation of a particular subset of CD4+ T cells at the onset of disease may be responsible for either progression or resolution of infection.

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