title: Selective inhibition of spontaneous IgE and IgG4 production by interleukin-8 in atopic patients.
abstract: The effects of interleukin (IL)-8 on spontaneous IgE and IgG4 production in atopic patients were studied. IL-8 inhibited IgE and IgG4 production by purified surface (s) IgE+ and sIgG4+ B cells, respectively, while it had no effect on IgG1, IgG2, IgG3, IgM, IgA1, and IgA2 production by corresponding sIg+ B cells. The IL-8-induced inhibition was counteracted by IL-6 and tumor necrosis factor-alpha (TNF-alpha) and was blocked by anti-IL-8 monoclonal antibody (MoAb). Conversely, the addition of anti-IL-6 MoAb and anti-TNF-alpha MoAb, in the absence of IL-8, inhibited IgE and IgG4 production by sIgE+ and sIgG4+ B cells, respectively. Purified sIgE+ and sIgG4+ B cells expressed IL-6 receptors (R), TNF-alpha R, and IL-8R, and they produced IL-6 and TNF-alpha, but not IL-8. IL-8 had no effect on IL-6R or TNF-alpha R, while it abrogated IL-6 and TNF-alpha production in these cells. In contrast, slgG1+, slgG2+, slgG2+, slgG3+, slgM+, slgA1+, and slgA2+ B cells expressed IL-6R and TNF-alpha R but not IL-8R, and they produced IL-6 and TNF-alpha. IL-8 had no effect on IL-6R and TNF-alpha R, or on TNF-alpha and IL-6 production in these cells. These results indicate that IL-8 inhibits spontaneous IgE and IgG4 production in slgE+ and slgG4+ B cells, respectively, by inhibiting the endogenous production of IL-6 and TNF-alpha.
authors.affiliation: Department of Pediatrics, Kyoto University Hospital, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kimata
authors.forename: I
authors.initials: I
authors.lastname: Lindley
authors.forename: K
authors.initials: K
authors.lastname: Furusho
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology; D016175:B-Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology; D004261:DNA Replication / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007073:Immunoglobulin E / Q000096:biosynthesis* / Q000235:genetics; D007074:Immunoglobulin G / Q000096:biosynthesis* / Q000235:genetics; D015850:Interleukin-6 / Q000494:pharmacology / Q000502:physiology*; D016209:Interleukin-8 / Q000494:pharmacology*; D011947:Receptors, Antigen, B-Cell / Q000032:analysis; D018121:Receptors, Cytokine / Q000096:biosynthesis / Q000235:genetics; D011994:Recombinant Proteins / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000502:physiology*; D000093242:Interleukin-6 Inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D007073:Immunoglobulin E; D007074:Immunoglobulin G; D015850:Interleukin-6; D016209:Interleukin-8; D011947:Receptors, Antigen, B-Cell; D018121:Receptors, Cytokine; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors