The role of B-cells and IgM antibodies in parasitemia, anemia, and VSG switching in Trypanosoma brucei-infected mice

Author Summary African trypanosomiasis is a disease caused by different species of extracellular flagellated protozoan trypanosome parasites. Trypanosomes have developed a mechanism of regular antigenic variation of their variant-specific surface glycoprotein (VSG) coat which allows chronic infection. Replacement of this coat occurs at rapid regular time intervals, allowing the parasite to escape from an effective host antibody responses. So far, primary T-cell independent antibody responses have been described to constitute the main host defense mechanism, relying largely on IgM antibody induction. Using genetically engineered B lymphocyte- or IgM-deficient mouse strains, we show that lack of B-cells or IgM did not prevent infection-associated anemia. More importantly, we show that in the absence of IgM, parasitemia was controlled almost as well as in wild-type mice, with only slightly increased mortality. In addition, we show in vivo that antigenic variation is not affected by the lack of IgM.