Mechanism of suppression of cell-mediated immunity by measles virus

被引：454

作者：

Karp, CL

Wysocka, M

Wahl, LM

Ahearn, JM

Cuomo, PJ

Sherry, B

Trinchieri, G

Griffin, DE

机构：

[1] WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104

[2] NIDR,IMMUNOL LAB,NIH,BETHESDA,MD 20892

[3] PICOWER INST MED RES,MANHASSET,NY 11030

[4] JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MOLEC MICROBIOL & IMMUNOL,BALTIMORE,MD 21205

来源：

SCIENCE | 1996年 / 273卷 / 5272期

关键词：

D O I：

10.1126/science.273.5272.228

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：228 / 231

页数：4

共 55 条

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[12] HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ACTIVATES THE CLASSICAL PATHWAY OF COMPLEMENT BY DIRECT C1-BINDING THROUGH SPECIFIC SITES IN THE TRANSMEMBRANE GLYCOPROTEIN-GP41 [J].