Rlk. Paterson et al., TRIGGERING THROUGH CD40 PROMOTES INTERLEUKIN-4-INDUCED CD23 PRODUCTION AND ENHANCED SOLUBLE CD23 RELEASE IN ATOPIC DISEASE, European Journal of Immunology, 26(9), 1996, pp. 1979-1984
The pathogenesis of atopic disease is closely linked to the overproduc
tion of IgE. CD23 and CD40 are two cellular receptors involved in the
regulation of IgE production and both receptors are elevated in atopic
disease. We have examined the role of CD40 in the regulation of CD23
and soluble CD23 production in healthy and atopic donors. Triggering o
f the B cell CD40 receptor directly enhances interleukin (IL)-4-mediat
ed up-regulation of CD23 at both the protein and the mRNA level. When
atopic donors were studied, the synergistic effect of CD40 triggering
on the IL-4-induced up-regulation of CD23 and soluble CD23 (sCD23) was
enhanced and there was a relative skewing toward production of sCD23.
These studies implicate the CD40 receptor in the hyperproduction of C
D23 and sCD23 in atopic disease and suggest that abnormalities may exi
st in the cellular pathways leading to sCD23 production.