title: IL-3 induces B7.2 (CD86) expression and costimulatory activity in human eosinophils.
abstract: 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 beta-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 beta-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.
authors.affiliation: Division of Immunology and Department of Pediatrics, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
authors.forename: J
authors.initials: J
authors.lastname: Celestin
authors.forename: O
authors.initials: O
authors.lastname: Rotschke
authors.forename: K
authors.initials: K
authors.lastname: Falk
authors.forename: N
authors.initials: N
authors.lastname: Ramesh
authors.forename: H
authors.initials: H
authors.lastname: Jabara
authors.forename: J
authors.initials: J
authors.lastname: Strominger
authors.forename: R S
authors.initials: RS
authors.lastname: Geha
mesh_terms: D000938:Antigen-Presenting Cells / Q000276:immunology / Q000378:metabolism; D000942:Antigens, Bacterial / Q000378:metabolism / Q000494:pharmacology; D015703:Antigens, CD / Q000096:biosynthesis* / Q000097:blood / Q000502:physiology; D051940:B7-2 Antigen; D002450:Cell Communication / Q000276:immunology; D002999:Clone Cells; D004306:Dose-Response Relationship, Immunologic; D004804:Eosinophils / Q000276:immunology* / Q000378:metabolism*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D007377:Interleukin-3 / Q000494:pharmacology*; D015848:Interleukin-5 / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000276:immunology; D008222:Lymphokines / Q000096:biosynthesis*; D008562:Membrane Glycoproteins / Q000096:biosynthesis* / Q000097:blood / Q000502:physiology; D010455:Peptides / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology; D015398:Signal Transduction / Q000276:immunology; D018089:Superantigens / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology; D013745:Tetanus Toxoid / Q000276:immunology / Q000378:metabolism
chemical_list: D000942:Antigens, Bacterial; D015703:Antigens, CD; D051940:B7-2 Antigen; C497964:CD86 protein, human; D007377:Interleukin-3; D015848:Interleukin-5; D008222:Lymphokines; D008562:Membrane Glycoproteins; D010455:Peptides; D018089:Superantigens; D013745:Tetanus Toxoid; C022227:eosinophil stimulating promoter; D016178:Granulocyte-Macrophage Colony-Stimulating Factor