title: Requirement of CD80 and CD86 molecules for antigen presentation by eosinophils.
abstract: The authors analysed the antigen-presenting ability of eosinophils purified from peritoneal exudate cells of interleukin-5 (IL-5) transgenic mice. The granulocyte-macrophage colony-stimulating factor (GM-CSF)-treated eosinophils induced proliferative responses of primed lymph node T cells and thymus T cells to staphylococcal enterotoxin B (SEB), while untreated eosinophils induced little or no response. GM-CSF-treated eosinophils also induced proliferation of ovalbumin (OVA)-primed lymph node T cells to OVA. Although untreated eosinophils expressed no MHC class II molecule on the surface the eosinophils could be induced to express major histocompatibility complex (MHC) class II molecules when treated with GM-CSF. In the present study, anti-I-Ak monoclonal antibodies (MoAbs) strongly inhibited proliferation of thymus T cells and proliferation of OVA-primed lymph node T cells in response to OVA, but weakly inhibited proliferation of primed T cells in response to SEB. Furthermore, CD80 (B7-1) and CD86 (B7-2) were expressed on the surfaces of untreated eosinophils. The expression of those two molecules on the eosinophils was increased by incubation with GM-CSF. Moreover, anti-CD80 or anti-CD86 MoAbs blocked proliferative responses of primed lymph node T cells and thymus T cells to SEB, and also blocked responses of primed lymph node T cells to OVA. Thus, CD80 and CD86 play an important role in stimulation of T cells by eosinophils.
authors.affiliation: Department of Dermatology, Yokohama City University School of Medicine, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Tamura
authors.forename: N
authors.initials: N
authors.lastname: Ishii
authors.forename: M
authors.initials: M
authors.lastname: Nakazawa
authors.forename: M
authors.initials: M
authors.lastname: Nagoya
authors.forename: M
authors.initials: M
authors.lastname: Yoshinari
authors.forename: T
authors.initials: T
authors.lastname: Amano
authors.forename: H
authors.initials: H
authors.lastname: Nakazima
authors.forename: M
authors.initials: M
authors.lastname: Minami
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D015703:Antigens, CD / Q000276:immunology*; D018122:B7-1 Antigen / Q000276:immunology*; D051940:B7-2 Antigen; D002455:Cell Division; D004768:Enterotoxins / Q000276:immunology; D004804:Eosinophils / Q000187:drug effects / Q000276:immunology*; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D015848:Interleukin-5 / Q000235:genetics; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology; D008562:Membrane Glycoproteins / Q000276:immunology*; D051379:Mice; D008809:Mice, Inbred C3H; D008822:Mice, Transgenic; D010047:Ovalbumin / Q000494:pharmacology; D018089:Superantigens / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology
chemical_list: D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; C497965:Cd86 protein, mouse; D004768:Enterotoxins; D000949:Histocompatibility Antigens Class II; D015848:Interleukin-5; D008562:Membrane Glycoproteins; D018089:Superantigens; C031818:enterotoxin B, staphylococcal; D010047:Ovalbumin