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

Item Type:Article
Title:IL-3 induces B7.2 (CD86) expression and costimulatory activity in human eosinophils
Creators Name:Celestin, J. and Roetzschke, O. and Falk, K. and Ramesh, N. and Jabara, H. and Strominger, J. and Geha, R.S.
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.
Keywords:Antigen-Presenting Cells, Bacterial Antigens, CD Antigens, CD86 Antigens, Cell Communication, Clone Cells, Eosinophils, Granulocyte-Macrophage Colony-Stimulating Factor, Immunologic Dose-Response Relationship, Interleukin-3, Interleukin-5, Lymphocyte Activation, Lymphokines, Membrane Glycoproteins, Peptides, Signal Transduction, Superantigens, T-Lymphocytes, Tetanus Toxoid
Source:Journal of Immunology
ISSN:0022-1767
Publisher:American Association of Immunologists (U.S.A.)
Volume:167
Number:11
Page Range:6097-6104
Date:1 December 2001
Official Publication:https://doi.org/10.4049/jimmunol.167.11.6097
PubMed:View item in PubMed

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