麻疹病毒抑制细胞介导免疫的机制。

Mechanism of suppression of cell-mediated immunity by measles virus.

作者信息

Karp C L, Wysocka M, Wahl L M, Ahearn J M, Cuomo P J, Sherry B, Trinchieri G, Griffin D E

机构信息

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

出版信息

Science. 1996 Jul 12;273(5272):228-31. doi: 10.1126/science.273.5272.228.

DOI:10.1126/science.273.5272.228

PMID:8662504

Abstract

The mechanisms underlying the profound suppression of cell-mediated immunity (CMI) accompanying measles are unclear. Interleukin-12 (IL-12), derived principally from monocytes and macrophages, is critical for the generation of CMI. Measles virus (MV) infection of primary human monocytes specifically down-regulated IL-12 production. Cross-linking of CD46, a complement regulatory protein that is the cellular receptor for MV, with antibody or with the complement activation product C3b similarly inhibited monocyte IL-12 production, providing a plausible mechanism for MV-induced immunosuppression. CD46 provides a regulatory link between the complement system and cellular immune responses.

摘要

伴随麻疹出现的细胞介导免疫（CMI）受到深度抑制的潜在机制尚不清楚。主要由单核细胞和巨噬细胞产生的白细胞介素-12（IL-12）对CMI的产生至关重要。麻疹病毒（MV）感染原代人单核细胞会特异性下调IL-12的产生。用抗体或补体激活产物C3b使CD46（一种作为MV细胞受体的补体调节蛋白）交联，同样会抑制单核细胞IL-12的产生，这为MV诱导的免疫抑制提供了一种合理的机制。CD46在补体系统和细胞免疫反应之间提供了一种调节联系。