title: Induction of IL-5 receptors on normal B cells by cross-linking surface Ig with anti-Ig-dextran.
abstract: Regulation of IL-5R expression in normal, non-Ly-1 (CD5) B cells was evaluated. Freshly isolated unfractionated spleen B cells express little or no detectable IL-5R. In contrast, B cells stimulated with anti-Ig-dextran conjugates express substantial numbers of IL-5R. Phenotypic analysis of the B cells responding to anti-Ig-dextran, and expressing IL-5R, demonstrates that these cells do not express Ly-1 or Mac-1. Scatchard analysis of B cells stimulated with anti-IgD-dextran reveals two classes of IL-5R: a high affinity receptor with a Kd of 17 pM and approximately 300 receptors/cell, and a low affinity receptor with a Kd of 0.6 nM and approximately 1000 receptors/cell. Peak receptor expression in response to anti-IgD-dextran is seen 72 h after stimulation and with a dose of 10 ng/ml. The induced receptors are functional, because both proliferation and Ig secretion by B cells treated with anti-IgD-dextran are enhanced by IL-5. Other B cell mitogens such as LPS, soluble anti-Ig/IL-4, or phorbol esters/ionomycin are poor inducers of the IL-5R. Finally, not only does LPS fail to induce significant IL-5R expression on spleen B cells, it suppresses both high and low affinity IL-5R expression induced by anti-IgD-dextran. These data indicate that normal, non-Ly-1 B cells are capable of expressing both high and low affinity IL-5R but that receptor expression is critically dependent on the type of stimulus provided to the B cell. A stimulus that produces extensive cross-linking of surface Ig on B cells, i.e., anti-Ig-dextran, is very effective in inducing IL-5R whereas a variety of other B cell mitogens are ineffective.
authors.affiliation: Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
authors.forename: K C
authors.initials: KC
authors.lastname: Allison
authors.forename: W
authors.initials: W
authors.lastname: Strober
authors.forename: G R
authors.initials: GR
authors.lastname: Harriman
mesh_terms: D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000502:physiology*; D000943:Antigens, Differentiation / Q000032:analysis; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D018956:CD5 Antigens; D003911:Dextrans / Q000008:administration & dosage*; D007072:Immunoglobulin D / Q000276:immunology; D015847:Interleukin-4 / Q000494:pharmacology; D015848:Interleukin-5 / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation; D016177:Macrophage-1 Antigen / Q000032:analysis; D051379:Mice; D008807:Mice, Inbred BALB C; D011947:Receptors, Antigen, B-Cell / Q000502:physiology*; D011971:Receptors, Immunologic / Q000096:biosynthesis*; D018123:Receptors, Interleukin; D053649:Receptors, Interleukin-5
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000943:Antigens, Differentiation; D018956:CD5 Antigens; D003911:Dextrans; D007072:Immunoglobulin D; D015848:Interleukin-5; D008070:Lipopolysaccharides; D016177:Macrophage-1 Antigen; D011947:Receptors, Antigen, B-Cell; D011971:Receptors, Immunologic; D018123:Receptors, Interleukin; D053649:Receptors, Interleukin-5; D015847:Interleukin-4