Free fatty acids, complement activation, and polyclonal B-cell stimulation as factors in the immunopathogenesis of African trypanosomiasis.

Human and animal forms of African trypanosomiasis are characterised by sustained hypocomplementaemia, gross hypergammaglobulinaemia M, and profound immunosuppression. It is suggested that this hypocomplementaemia is probably due to the action of a trypanosome-derived complement-activating factor and that the elevated IgM levels may be the combined result of this decomplementation, together with a subsequent failure of the normal IgM-to-IgG antibody switch mechanism and polyclonal B-lymphocyte activation by a trypanosome-generated mitogen. The immunosuppression in this disease may be a result of the collective immunosuppressive effects of trypanosome-derived immune-modulating free fatty acids, polyclonally stimulating B-cell mitogen, and complement-activating factors.