title: Histamine selectively enhances human immunoglobulin E (IgE) and IgG4 production induced by anti-CD58 monoclonal antibody.
abstract: We studied the effects of histamine on human immunoglobulin (IgE) and IgG4 production. Histamine selectively enhanced IgE and IgG4 production in purified surface IgE and IgG4 negative (sIgE-sIgG4-) B cells from normal donors stimulated with interleukin (IL)-4 plus anti-CD58 or IL-13 plus anti-CD58 monoclonal antibody (mAb) without affecting production of IgG1, IgG2, IgG3, IgM, IgA1, or IgA2. In cultures with IL-4 plus anti-CD58 mAb, histamine-induced enhancement of IgE and IgG4 production was specifically blocked by thioperamide (H3 receptor antagonist), and was inhibited by anti-IL-10 antibody (Ab). In contrast, in cultures with IL-13 plus anti-CD58 mAb, histamine-induced enhancement was blocked by dimaprit (H1 receptor antagonist), and was inhibited by anti-IL-6 mAb. Histamine also enhanced IgE and IgG4 production by in vivo-generated sIgE+ and sIgG4+ B cells, respectively, from atopic patients; enhancement was blocked by dimaprit and thioperamide, and was inhibited by anti-IL-6 mAb and anti-IL-10 Ab. In sIgE-sIgG4- B cells, IL-4 plus anti-CD58 mAb induced IL-10 production and IL-10 receptor expression, whereas IL-13 plus anti-CD58 mAb induced IL-6 production and IL-6 receptor expression. Histamine increased IL-10 and IL-6 production without affecting IL-10 and IL-6 receptor expression, in cultures with IL-4 plus anti-CD58 mAb and with IL-13 plus anti-CD58 mAb, respectively, which was blocked by thioperamide and dimaprit, respectively. In contrast, sIgE+ and sIgG4+ B cells spontaneously produced both IL-6 and IL-10 and constitutively expressed IL-6 and IL-10 receptors, and histamine increased IL-6 and IL-10 production without affecting IL-6 or IL-10 receptor expression, which was blocked by thioperamide and dimaprit. These results indicate that histamine enhanced IgE and IgG4 production by increasing endogenous IL-6 and IL-10 production via H1 and H3 receptors, respectively.
authors: Department of Pediatrics, Unitika Central Hospital, Kyoto, Japan.
authors: H
authors: H
authors: Kimata
authors: M
authors: M
authors: Fujimoto
authors: C
authors: C
authors: Ishioka
authors: A
authors: A
authors: Yoshida
mesh_terms: D000911:Antibodies, Monoclonal; D016175:B-Lymphocyte Subsets / Q000378:metabolism*; D018968:CD58 Antigens / Q000502:physiology*; D002478:Cells, Cultured; D006632:Histamine / Q000008:administration & dosage*; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007074:Immunoglobulin G / Q000096:biosynthesis*; D016753:Interleukin-10 / Q000378:metabolism; D018793:Interleukin-13 / Q000008:administration & dosage; D015850:Interleukin-6 / Q000378:metabolism; D014066:Palatine Tonsil / Q000166:cytology; D011969:Receptors, Histamine H1 / Q000378:metabolism; D011970:Receptors, Histamine H2 / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D018968:CD58 Antigens; D007074:Immunoglobulin G; D018793:Interleukin-13; D015850:Interleukin-6; D011969:Receptors, Histamine H1; D011970:Receptors, Histamine H2; D016753:Interleukin-10; D007073:Immunoglobulin E; D006632:Histamine