THE EFFECT OF DISODIUM-CROMOGLYCATE (DSCG) ON IN-VITRO PROLIFERATION OF CD4(-POPULATIONS DERIVED FROM ALLERGIC AND HEALTHY DONORS() CD8(+),AND CD19(+) CELL)

Authors
Citation
E. Holen et S. Elsayed, THE EFFECT OF DISODIUM-CROMOGLYCATE (DSCG) ON IN-VITRO PROLIFERATION OF CD4(-POPULATIONS DERIVED FROM ALLERGIC AND HEALTHY DONORS() CD8(+),AND CD19(+) CELL), Allergy, 50(3), 1995, pp. 249-256
Citations number
39
Categorie Soggetti
Allergy
Journal title
ISSN journal
01054538
Volume
50
Issue
3
Year of publication
1995
Pages
249 - 256
Database
ISI
SICI code
0105-4538(1995)50:3<249:TEOD(O>2.0.ZU;2-B
Abstract
The effect of disodium cromoglycate (DSCG) on in vitro proliferation o f CD4(+) and CD8(+) T cells and CD19(+) B cells, positively selected b y immunomagnetic separation, was investigated. The cells were obtained from allergic patients with moderate serum IgE levels and mild to mod erate atopic dermatitis, and healthy controls. The different cell subf ractions were stimulated with mitogens or specific allergens, as well as cell supernatants from the lymphoblastoid B- (RPMI 8866) and T-hybr idoma (166 A(2)) 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 alle rgic individuals, significant allergen-specific stimulation could be o bserved in the CD8-depleted peripheral blood mononuclear cell (PBMC) f ractions. Isolated CD4(+) T cells, without AC or IL-2, could also be s timulated with specific allergen, but the responses were rather low. D SCG inhibited, concentration dependently, all allergen-induced respons es. 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, prese nt in culture supernatants from RPMI 8866 and 166 A(2), respectively. These responses were also inhibited by DSCG. This was in contrast to t he amplifying effect of DSCG on spontaneously proliferating RPMI 8866 and 166 A(2) cells, cultured in fresh cRPMI 1640 medium without sCD23 and IgE enhancing factor. Our results show that DSCG delivers an inhib itory signal or signals to PBMC subpopulations expressing Fc(epsilon)R II/sCD23, either upregulated by phytohemagglutinin in normal and atopi c cells, or by allergens or sCD23 in atopic cells. The findings sugges t that sCD23 in supernatants or in serum may reverse the general inhib itory mode of DSCG.