IL-3 induces B7.2 (CD86) expression and costimulatory activity in human eosinophils

Eosinophils in tissues are often present in intimate contact with T cells i n allergic and parasitic diseases. Resting eosinophils do not express MHC c lass II proteins or costimulatory B7 molecules and fail to induce prolifera tion of T cells to Ags. IL-5 and GM-CSF induce MHC class If and B7 expressi on on eosinophils and have been reported in some studies to induce eosinoph ils to present Ag to T cells. The cytokine IL-3, like IL-5 and GM-CSF, is a survival and activating factor for eosinophils; and the IL-3 receptor shar es with the IL-5 and GM-CSF receptors a common signal transducing beta -cha in. IL-3-treated eosinophils expressed HLA-DR and B7.2, but not B7.1 on the ir surface and supported T cell proliferation in response to the superantig en toxic shock syndrome toxin 1, as well as the proliferation of HLA-DR-res tricted tetanus toxoid (TT) and influenza hemagglutinin-specific T cell clo nes to antigenic peptides. This was inhibited by anti-B7.2 mAb. In contrast , IL-3-treated eosinophils were unable to present native TT Ag to either re sting or TT-specific cloned T cells. In parallel experiments, eosinophils t reated with IL-5 or GM-CSF were also found to present superantigen and anti genic peptides, but not native Ag, to T cells. These results suggest that e osinophils are deficient in Ag processing and that this deficiency is not o vercome by cytokines that signal via the beta -chain. Nevertheless, our fin dings suggest that eosinophils activated by IL-3 may contribute to T cell a ctivation in allergic and parasitic diseases by presenting superantigens an d peptides to T cells.