title: Respiratory burst in human B lymphocytes. Triggering of surface Ig receptors induces modulation of chemiluminescence signal.
abstract: B lymphocytes have been shown to proliferate and release oxygen metabolites when surface Ig is cross-linked and when stimulated with phorbol ester. Biochemical evidence has been provided for the presence of a superoxide generating system in B cells, which seems to be identical to the well-characterized NADPH-oxidase of phagocytes. In this report, we show that normal and EBV-transformed B cells produce superoxide anions after stimulation with phorbol ester and when surface Ig was cross-linked, as detected by lucigenin-dependent chemiluminescence. Anti-surface IgG antibodies induced a significant respiratory burst whereas those directed against surface IgM had no effect on B cell oxidative metabolism. Prestimulated B lymphocytes responded to further triggering by the same or another ligand. Pretreatment with Staphlococcus aureus Cowan I strain (SAC) or anti-IgM antibodies resulted in complete unresponsiveness to subsequent SAC or anti-IgG stimulation, but it did not affect PMA- and ionomycin-mediated B cell chemiluminescence. In contrast to preincubation with anti-IgM antibodies, the pretreatment of B cells with SAC induced a transient inhibitory effect on B cell signaling. In fact, SAC-pretreated B lymphocytes could be restimulated with the same ligand when blast cells were isolated. Furthermore, a 24-h incubation of the pretreated B cells in the absence of SAC completely restored the SAC-mediated respiratory burst. These results suggest that two distinct mechanisms may account for SAC- and anti-IgM-induced inhibition: a transient and reversible modulation of surface Ig, induced by SAC, and a long-lasting desensitization of the surface Ig receptors, respectively. These findings may have interesting implications for understanding the transduction of negative signals in B lymphocytes.
authors.affiliation: INSERM U 131, Clamart, France.
authors.forename: G
authors.initials: G
authors.lastname: Leca
authors.forename: G
authors.initials: G
authors.lastname: Benichou
authors.forename: A
authors.initials: A
authors.lastname: Bensussan
authors.forename: F
authors.initials: F
authors.lastname: Mitenne
authors.forename: P
authors.initials: P
authors.lastname: Galanaud
authors.forename: A
authors.initials: A
authors.lastname: Vazquez
mesh_terms: D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D001402:B-Lymphocytes / Q000378:metabolism*; D002460:Cell Line; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D015759:Ionomycin / Q000494:pharmacology; D008163:Luminescent Measurements; D009000:Monocytes / Q000378:metabolism; D011947:Receptors, Antigen, B-Cell / Q000378:metabolism*; D011971:Receptors, Immunologic / Q000502:physiology*; D015398:Signal Transduction; D013211:Staphylococcus aureus / Q000276:immunology; D013481:Superoxides / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D000888:Antibodies, Anti-Idiotypic; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D011947:Receptors, Antigen, B-Cell; D011971:Receptors, Immunologic; D013481:Superoxides; D015759:Ionomycin; D013755:Tetradecanoylphorbol Acetate