SummaryMice from lines genetically selected for the production of either high or low affinity antibody to protein antigens and which differ in their susceptibility to chronic immune complex disease were infected withTrypanosoma musculi.The parasite became patent in both lines by day 5 and no significant differences in the levels of parasites during the infection were observed between the two lines. Serum levels of both antigen non‐specific andT. musculiantigen specific immune complexes were determined during the infection by the solid phase conglutinin and C1qbinding assays. In both lines, antigen non‐specific complexes were detected by day 15 after infection with maximum levels observed by day 30. At this time, low affinity line mice had significantly higher levels than did high line mice as determined by the C1qassay but not by the conglutinin assay. The deposition of immune complex like material in glomeruli, assessed by immunofluorescence, was associated with the clearance of the parasite and the presence of circulating antigen specific complexes. The pattern of localization of complexes in both lines was predominantly mesangial with some deposition in the capillaries. The intensity of fluorescence increased during the infection. Initially (day 10) only IgM was observed in the glomeruli but IgGl and IgG2b were detected from day 20 to day 40. IgG2a was only detected on day 40. However, in none of the animals was this deposition of complexes associated with proteinuria. Hence, the data presented here show that the low affinity line mice produce higher levels of smaller circulating complexes followingT. musculiinfection than do high affinity mice. However, this does not result in significant differences in localization and induction of renal disease as seen following chronic antigen inject