The Journal of Immunology, Vol 152, Issue 5 2139-2147, Copyright © 1994 by American Association of Immunologists

ARTICLES

Regulation of CD23 expression by IL-4 and corticosteroid in human B lymphocytes. Altered response after EBV infection

RL Paterson, R Or, JM Domenico, G Delespesse and EW Gelfand
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.

Cellular CD23 has been implicated in various biologic and pathologic processes. Here, we have studied the regulation of B cell CD23 expression and function by the synthetic corticosteroid, dexamethasone (DEX). We report that DEX acts directly on B lymphocytes to down- regulate IL-4-induced CD23 expression, whereas in parallel the IL-4R is up-regulated. Down-regulation of CD23 occurred at the cell surface and for shed material in culture medium. EBV infection of B cells is linked to development of lymphoproliferative diseases, including lymphoma, and there is evidence that EBV-stimulated CD23 expression may be instrumental in the inappropriate survival of infected cells. We have determined that treatment of EBV-infected cells with IL-4 leads to a synergistic up-regulation of B cell CD23. Furthermore, infection of B cells by EBV introduced a relative resistance to the down-regulatory effects of DEX on IL-4-induced CD23 expression.

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