SOLUBLE CD23 POTENTIATES INTERLEUKIN-1-INDUCED SECRETION OF INTERLEUKIN-6 AND INTERLEUKIN-1 RECEPTOR ANTAGONIST BY HUMAN MONOCYTES

The low-affinity receptor for IgE (CD23) is cleaved into biologically active soluble fragments (sCD23), some of which have been reported to exhibit pleiotropic activities. However, it is not known whether the s CD23 fragments contribute to the induction and/or regulation of pro-in flammatory cytokine production. In this study, this possibility was te sted using interleukin (IL)-1-stimulated human whole blood as an ex vi vo model of cytokine cascade production. We show that human recombinan t 25-kDa sCD23 significantly enhanced the production of IL-6 in whole blood stimulated by IL-1, but had only little or no effect in the abse nce of IL-1. The potentiating effect of sCD23 was concentration depend ent within the range of plasma levels occurring during various inflamm atory processes in man. These results prompted us to study whether sCD 23 and IL-1 together also enhance the production of regulating factors exhibiting anti-cytokine activities. Our data indicate that sCD23 aug ments the release of IL-1 receptor antagonist induced by IL-1. Finall y, examining the effect of sCD23 on human peripheral monocytes stimula ted by IL-1, we confirmed the capacity of sCD23 to potentiate cytokine production. We suggest that sCD23 can modulate monocyte functions, th ereby contributing to the amplification and regulation of immune and i nflammatory processes.