Memory CD4+ T cells induce innate responses independently of pathogen

被引：148

作者：

Strutt, Tara M. ^{[1
]}

McKinstry, K. Kai ^{[1
]}

Dibble, John P. ^{[1
]}

Winchell, Caylin ^{[1
]}

Kuang, Yi ^{[1
]}

Curtis, Jonathan D. ^{[1
]}

Huston, Gail ^{[1
]}

Dutton, Richard W. ^{[1
]}

Swain, Susan L. ^{[1
]}

机构：

[1] Trudeau Inst Inc, Saranac Lake, NY 12983 USA

来源：

NATURE MEDICINE | 2010年 / 16卷 / 05期

基金：

美国国家卫生研究院;

关键词：

INFLUENZA-A; ANTIVIRAL RESPONSES; PROTECTIVE IMMUNITY; VIRAL-INFECTIONS; IFN-GAMMA; ACTIVATION; CD8(+); INTERLEUKIN-12; GENERATION; CHEMOKINES;

D O I：

10.1038/nm.2142

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses. We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses. We found that the response of memory, but not naive, CD4(+) T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus. Memory CD4(+) T cell-induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (T(H)1) or T(H)17 polarized but are independent of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) production and do not require activation of conserved pathogen recognition pathways. This represents a previously undescribed mechanism by which memory CD4(+) T cells induce an early innate response that enhances immune protection against pathogens.

引用

页码：558 / U91

页数：8

共 50 条

[1]

Amichay D, 1996, J IMMUNOL, V157, P4511

[2] Cellular responses to interferon-gamma [J].