Dendritic cells respond to influenza virus through TLR7- and PKR-independent pathways

被引：96

作者：

Barchet, W

Krug, A

Cella, M

Newby, C

Fischer, JAA

Dzionek, A

Pekosz, A

Colonna, M ^{[1
]}

机构：

[1] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Dept Microbiol, St Louis, MO 63110 USA

[3] Miltenyi Biotec, Bergisch Gladbach, Germany

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 2005年 / 35卷 / 01期

关键词：

dendritic cell; viral; interferon-alpha;

D O I：

10.1002/eji.200425583

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Natural interferon-producing cells (IPC) secrete type I IFN (IFN-alpha and -beta) in response to influenza virus. This process is independent of viral replication and is mediated by Toll-like receptor 7 (TLR7), which recognizes single-stranded RNA (ssRNA). DC also express TLR7 but its function in DC response to influenza virus is unknown. To address this, we compared the DC and IPC responses to influenza virus and ssRNA oligoribonucleotides (ORN) that activate TLR7. When stimulated by ORN in vitro and in vivo, DC matured and produced inflammatory cytokines but not IFN-alpha. DC did secrete IFN-alpha in response to influenza virus. However, this response was independent of TLR7 signaling and required viral replication but not dsRNA-activated protein kinase (PKR). We conclude that DC and IPC are hard-wired to secrete IFN-alpha via different pathways, reflecting their complementary but distinct roles in anti-viral immunity.

引用

页码：236 / 242

页数：7

共 29 条

[1] Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function [J].