title: alpha-galactosylceramide induces early B-cell activation through IL-4 production by NKT cells.
abstract: alpha-Galactosylceramide (alpha-GalCer), a glycolipid antigen, specifically activates natural killer T (NKT) cells by a CD1d-restricted mechanism. In this work, we found that in vivo administration of alpha-GalCer resulted in the activation of B cells in addition to NKT cells, namely, alpha-GalCer administration caused upregulation of the early activation marker, CD69, on both NKT and B cells. In addition, expression of B7.2 and I-A(b) on B cells was greatly upregulated by alpha-GalCer. However, serum levels of IgE, IgG1, and IgG2a were not significantly changed within 48 h. In the present experiments, it was also demonstrated that the upregulation of CD69 expression by alpha-GalCer was strongly blocked by anti-IL-4 monoclonal antibody. Moreover, B-cell activation by alpha-GalCer was not observed in NKT-deficient mice. These results suggested that antigen-stimulated NKT cells might play a critical role not only in early defense mechanisms but also in early B-cell activation through IL-4 production.
authors.affiliation: Section of Genetic Engineering, Tokai University School of Medicine, Bohseidai, Isehara, 259-1193, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kitamura
authors.forename: A
authors.initials: A
authors.lastname: Ohta
authors.forename: M
authors.initials: M
authors.lastname: Sekimoto
authors.forename: M
authors.initials: M
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Iwakabe
authors.forename: M
authors.initials: M
authors.lastname: Nakui
authors.forename: T
authors.initials: T
authors.lastname: Yahata
authors.forename: H
authors.initials: H
authors.lastname: Meng
authors.forename: T
authors.initials: T
authors.lastname: Koda
authors.forename: S
authors.initials: S
authors.lastname: Nishimura
authors.forename: T
authors.initials: T
authors.lastname: Kawano
authors.forename: M
authors.initials: M
authors.lastname: Taniguchi
authors.forename: T
authors.initials: T
authors.lastname: Nishimura
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D000941:Antigens / Q000008:administration & dosage / Q000276:immunology; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured; D018920:Coculture Techniques; D005699:Galactosylceramides / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000276:immunology*; D017353:Gene Deletion; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000097:blood; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000097:blood; D007371:Interferon-gamma / Q000096:biosynthesis / Q000097:blood / Q000276:immunology; D015847:Interleukin-4 / Q000096:biosynthesis* / Q000097:blood; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism; D037181:Lectins, C-Type; D008213:Lymphocyte Activation / Q000276:immunology*; D016131:Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D011948:Receptors, Antigen, T-Cell / Q000276:immunology; D011971:Receptors, Immunologic / Q000276:immunology; D015854:Up-Regulation / Q000187:drug effects; D000099192:CD69 Antigens
chemical_list: D000911:Antibodies, Monoclonal; D000941:Antigens; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D005699:Galactosylceramides; D007073:Immunoglobulin E; D007074:Immunoglobulin G; D007371:Interferon-gamma; D015847:Interleukin-4; D037181:Lectins, C-Type; D011948:Receptors, Antigen, T-Cell; D011971:Receptors, Immunologic; D000099192:CD69 Antigens; C489917:Nktr protein, mouse