title: Soluble, but not immobilized, anti-IgM antibody inhibits post-activation events leading to T-cell-dependent B-cell differentiation.
abstract: The potential for surface immunoglobulin-binding ligands to modify B-cell differentiation responses induced by activated T cells has been investigated. Activated T cells in human splenic mononuclear cells cultured on anti-CD3-coated plates induced B cells to produce large amounts of IgM and IgG. In this experimental system, cross-linking of B-cell antigen receptors by soluble, bivalent monoclonal or polyclonal anti-IgM antibodies completely inhibited IgM production, and greatly diminished IgG production, in a dose-dependent manner. Similar results were obtained using a F(ab')2 fragment of a goat anti-IgM antibody. Inhibition of B-cell differentiation by bivalent cross-linking reagents did not require the presence of antigen-presenting cells (APC), as comparable results were obtained in co-cultures of purified T and B cells. In contrast, enhanced immunoglobulin secretion was seen when surface IgM was cross-linked using anti-IgM antibody immobilized on the culture plate. Interestingly, activated T cells induced similar levels of expression on B cells of the activation antigens CD23, CD25 and CD71, and of class II molecules, irrespective of any treatment with soluble or immobilized anti-IgM antibody. This indicates that soluble anti-IgM specifically inhibits B-cell differentiation without altering initial events of T-cell-dependent B-cell activation.
authors.affiliation: Department of Immunology, Hospital Central de Asturias, Centro Universitario, Oviedo, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Zamorano
authors.forename: D
authors.initials: D
authors.lastname: Rivas
authors.forename: A
authors.initials: A
authors.lastname: Gayo
authors.forename: L
authors.initials: L
authors.lastname: Mozo
authors.forename: C
authors.initials: C
authors.lastname: Gutiérrez
mesh_terms: D000888:Antibodies, Anti-Idiotypic / Q000502:physiology*; D015703:Antigens, CD / Q000276:immunology; D000944:Antigens, Differentiation, B-Lymphocyte / Q000276:immunology; D001402:B-Lymphocytes / Q000166:cytology* / Q000276:immunology; D015153:Blotting, Western; D004306:Dose-Response Relationship, Immunologic; D006681:HLA-D Antigens / Q000276:immunology; D006801:Humans; D007075:Immunoglobulin M; D008213:Lymphocyte Activation; D011947:Receptors, Antigen, B-Cell / Q000276:immunology*; D017455:Receptors, IgE / Q000276:immunology; D015375:Receptors, Interleukin-2 / Q000276:immunology; D011990:Receptors, Transferrin; D012995:Solubility; D013601:T-Lymphocytes / Q000166:cytology* / Q000276:immunology; D015854:Up-Regulation
chemical_list: D000888:Antibodies, Anti-Idiotypic; D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; C068126:CD71 antigen; D006681:HLA-D Antigens; D007075:Immunoglobulin M; D011947:Receptors, Antigen, B-Cell; D017455:Receptors, IgE; D015375:Receptors, Interleukin-2; D011990:Receptors, Transferrin