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Division of Immunology and Department of Pediatrics, Children’s Hospital, Harvard Medical School, Boston, MA 02115; and
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138
Eosinophils in tissues are often present in intimate contact with T
cells in allergic and parasitic diseases. Resting eosinophils do not
express MHC class II proteins or costimulatory B7 molecules and fail to
induce proliferation of T cells to Ags. IL-5 and GM-CSF induce MHC
class II and B7 expression on eosinophils and have been reported in
some studies to induce eosinophils 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 shares with the IL-5 and
GM-CSF receptors a common signal transducing 
-chain. IL-3-treated
eosinophils expressed HLA-DR and B7.2, but not B7.1 on their surface
and supported T cell proliferation in response to the superantigen
toxic shock syndrome toxin 1, as well as the proliferation of
HLA-DR-restricted tetanus toxoid (TT) and influenza
hemagglutinin-specific T cell clones 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 resting or TT-specific
cloned T cells. In parallel experiments, eosinophils treated with IL-5
or GM-CSF were also found to present superantigen and antigenic
peptides, but not native Ag, to T cells. These results suggest that
eosinophils are deficient in Ag processing and that this deficiency is
not overcome by cytokines that signal via the -chain. Nevertheless,
our findings suggest that eosinophils activated by IL-3 may contribute
to T cell activation in allergic and parasitic diseases by presenting
superantigens and peptides to T cells.
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