AbstractIn previous studies, it was shown that mice infected withPlasmodium chabaudi adamihave a deficiency in their production of IgG1immunoglobulin, suggesting isotype‐specific immunoregulation. In order to examine this phenomenon in further detail the expression of Fcγreceptors (FcγR) on T cells obtained from mice infected withP. chabaudiwas studied by flow cytometry. There was an increase in the number of splenic T cells which expressed FcγR during infection. At the peak of the acute stage of infection (10–15 days) up to 40% of T cells were positive for FcγR expression. These FcγR were present on about 40% of both Lyt‐2+and L3T4+T cells. The isotype preference of these receptors on control Thy‐l+T cells is IgG1IgG2b>IgG2a as determined by an inhibition assay and fluorescence‐activated cell sorter (FACS) analysis. However, 2 to 3 weeks after infection this pattern was altered such that IgG2band IgG2arepresented the major isotypes binding to the FcγR of the L3T4+T cell. At this stage of infection FcγR on L3T4+cells fail to bind IgG1. In the Lyt‐2+T cells IgG1and IgG2bremained the best inhibitors. These data suggest that there may be changes in FcγR expression on T cells during infection reflected particularly in a decreased ability of IgG1to bind to the