title: The effect of disodium cromoglycate (DSCG) on in vitro proliferation of CD4+, CD8+, and CD19+ cell populations derived from allergic and healthy donors.
abstract: The effect of disodium cromoglycate (DSCG) on in vitro proliferation of CD4+ and CD8+ T cells and CD19+ B cells, positively selected by immunomagnetic separation, was investigated. The cells were obtained from allergic patients with moderate serum IgE levels and mild to moderate atopic dermatitis, and healthy controls. The different cell subfractions were stimulated with mitogens or specific allergens, as well as cell supernatants from the lymphoblastoid B- (RPMI 8866) and T-hybridoma (166 A2) cell lines. Proliferative responses of T- and B-cell subsets stimulated with mitogens together with recombinant interleukin-2 (rIL-2) or accessory cells (AC) could be inhibited by DSCG. In allergic individuals, significant allergen-specific stimulation could be observed in the CD8-depleted peripheral blood mononuclear cell (PBMC) fractions. Isolated CD4+ T cells, without AC or IL-2, could also be stimulated with specific allergen, but the responses were rather low. DSCG inhibited, concentration dependently, all allergen-induced responses. Interestingly, only atopic derived CD4+ and CD8+ T cells were stimulated by soluble low-affinity IgE receptor (Fc epsilon RII/sCD23) and IgE binding factor (IgEBF), including IgE enhancing factor, present in culture supernatants from RPMI 8866 and 166 A2, respectively. These responses were also inhibited by DSCG. This was in contrast to the amplifying effect of DSCG on spontaneously proliferating RPMI 8866 and 166 A2 cells, cultured in fresh cRPMI 1640 medium without sCD23 and IgE enhancing factor. Our results show that DSCG delivers an inhibitory signal or signals to PBMC subpopulations expressing Fc epsilon RII/sCD23, either upregulated by phytohemagglutinin in normal and atopic cells, or by allergens or sCD23 in atopic cells.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Clinical Biology, Haukeland Hospital, University of Bergen, Norway.
authors.forename: E
authors.initials: E
authors.lastname: Holen
authors.forename: S
authors.initials: S
authors.lastname: Elsayed
mesh_terms: D000485:Allergens / Q000494:pharmacology; D015703:Antigens, CD / Q000276:immunology; D018941:Antigens, CD19; D000944:Antigens, Differentiation, B-Lymphocyte / Q000276:immunology; D016175:B-Lymphocyte Subsets / Q000187:drug effects; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects; D016022:Case-Control Studies; D002478:Cells, Cultured; D004205:Cromolyn Sodium / Q000494:pharmacology*; D017077:Culture Media, Conditioned / Q000494:pharmacology; D003876:Dermatitis, Atopic / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D016131:Lymphocyte Subsets / Q000187:drug effects*; D008934:Mitogens / Q000494:pharmacology
chemical_list: D000485:Allergens; D015703:Antigens, CD; D018941:Antigens, CD19; D000944:Antigens, Differentiation, B-Lymphocyte; D017077:Culture Media, Conditioned; D008934:Mitogens; D004205:Cromolyn Sodium