Expression of Fc gamma receptors on splenic T cells of mice infected with Plasmodium chabaudi adami.

In previous studies, it was shown that mice infected with Plasmodium chabaudi adami have a deficiency in their production of IgG1 immunoglobulin, suggesting isotype-specific immunoregulation. In order to examine this phenomenon in further detail the expression of Fc gamma receptors (Fc gamma R) on T cells obtained from mice infected with P. chabaudi was studied by flow cytometry. There was an increase in the number of splenic T cells which expressed Fc gamma R during infection. At the peak of the acute stage of infection (10-15 days) up to 40% of T cells were positive for Fc gamma R expression. These Fc gamma R were present on about 40% of both Lyt-2+ and L3T4+T cells. The isotype preference of these receptors on control Thy-1+ T cells is IgG1 greater than IgG2b greater than 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 IgG2b and IgG2a represented the major isotypes binding to the Fc gamma R of the L3T4+ T cell. At this stage of infection Fc gamma R on L3T4+ cells fail to bind IgG1. In the Lyt-2% T cells IgG1 and IgG2b remained the best inhibitors. These data suggest that there may be changes in Fc gamma R expression on T cells during infection reflected particularly in a decreased ability of IgG1 to bind to the Fc gamma R of L3T4+ cells.