Paterson R L, Or R, Domenico J M, Delespesse G, Gelfand E W
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.
J Immunol. 1994 Mar 1;152(5):2139-47.
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.
细胞表面的CD23参与了多种生物学和病理学过程。在此，我们研究了合成皮质类固醇地塞米松（DEX）对B细胞CD23表达和功能的调节作用。我们报告称，DEX直接作用于B淋巴细胞，下调IL-4诱导的CD23表达，与此同时上调IL-4R。CD23的下调发生在细胞表面以及培养基中的脱落物质上。B细胞的EB病毒感染与包括淋巴瘤在内的淋巴增殖性疾病的发生有关，并且有证据表明EB病毒刺激的CD23表达可能有助于受感染细胞的异常存活。我们已经确定，用IL-4处理EB病毒感染的细胞会导致B细胞CD23的协同上调。此外，EB病毒对B细胞的感染使细胞对DEX对IL-4诱导的CD23表达的下调作用产生了相对抗性。
