Trypanosoma brucei brucei infection impairs MHC class II antigen presentation capacity of macrophages

During African trypanosomiasis, macrophages play a central role in T cell h yporesponsiveness to parasite-related and unrelated antigens. In this study , the ability of macrophages from Trypanosoma b. brucei-infected mice to pr esent exogenous antigens to a major histocompatibility complex (MHC) class II-restricted CD4(+) T cell hybridoma was analysed. We demonstrate that the antigen presentation capacity of macrophages from infected mice is markedl y reduced as a result of a lower expression of [MHC class II-peptide] compl exes on their plasma membrane. This defect did not result from a decreased antigen uptake/catabolism, a reduced MHC class II and intercellular adhesio n molecule 1 expression on the surface of macrophages, a decreased affinity of MHC class II molecules for antigenic peptides, a competition between ex ogenous and parasite antigens, or the generation of inhibitory peptides. Ou r data indicate that the step resulting in coexpression of processed antige ns and MHC class II molecules is affected in T. b. brucei-infected mice. Ad ditionally, macrophages from infected mice secreted IL-10 that in turn cont ributes to the impairment of T cell activation.