Trypanosome infection of mice depresses antibody affinity and delays affinity maturation.

Infection with either a pathogenic species of trypanosome (Trypanosoma brucei brucei) or a non-pathogenic trypanosome (Trypanosoma musculi) had differing effects on the response of mice to a soluble protein antigen (human serum albumin, HSA) injected in either Freund's incomplete adjuvant or in saline. T. brucei suppressed the response to HSA to a level undetectable by ammonium sulphate globulin precipitation, irrespective of the mode of immunization, whereas T. musculi did not suppress the amount of antibody produced in response to either form of antigen presentation. The affinity of the antibody produced in response to antigen in adjuvant was unaffected, but antibody affinity was significantly reduced in infected animals in which the antigen was given in saline. This depression of antibody affinity was related to the period of infection and arose as a result of a delay in the normal maturation of affinity. Furthermore, the depression was only observed when infection preceded the exposure to antigen. Possible mechanisms which may lead to a depression of affinity without a corresponding effect upon antibody levels are discussed in context of current knowledge of immunosuppression in trypanosome infections.