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