Autocrine activation of microglia by tumor necrosis factor-α

被引：181

作者：

Kuno, R ^{[1
]}

Wang, JY ^{[1
]}

Kawanokuchi, J ^{[1
]}

Takeuchi, H ^{[1
]}

Mizuno, T ^{[1
]}

Suzumura, A ^{[1
]}

机构：

[1] Nagoya Univ, Inst Environm Med, Dept Neuroimmunol, Chikusa Ku, Nagoya, Aichi 4648601, Japan

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2005年 / 162卷 / 1-2期

关键词：

microglia; tumor necrosis factor-alpha (TNF-alpha); TNFR1(p55); TNFR2(p75);

D O I：

10.1016/j.jneuroim.2005.01.015

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

In the central nervous system (CNS), tumor necrosis factor-alpha (TNF-alpha) derived from activated microglia plays a critical role as an inflammatory mediator. In this study, we examined the function of TNF-alpha as an autocrine mediator in microglial activation. TNF-alpha induced TNF-alpha production by microglia through ligation of TNF receptor 1 (TNFR1). TNF-alpha also increased the production of other inflammatory mediators. The activation of microglia by lipopolysaccharide is partially mediated by microglia-derived TNF-alpha. These findings suggest the existence of a positive feedback loop in the activation of microglia via TNF-alpha. This autocrine loop may be involved in the prolonged activation of microglia. (C) 2005 Elsevier B.V All rights reserved.

引用

页码：89 / 96

页数：8

共 45 条

[1] The peripheral benzodiazepine binding site in the brain in multiple sclerosis -: Quantitative in vivo imaging of microglia as a measure of disease activity [J].

Banati, RB ;

Newcombe, J ;

Gunn, RN ;

Cagnin, A ;

Turkheimer, F ;

Heppner, F ;

Price, G ;

Wegner, F ;

Giovannoni, G ;

Miller, DH ;

Perkin, GD ;

Smith, T ;

Hewson, AK ;

Bydder, G ;

Kreutzberg, GW ;

Jones, T ;

Cuzner, ML ;

Myers, R .

BRAIN, 2000, 123 :2321-2337

[2] Inflammation and degeneration in multiple sclerosis [J].

Brück, W ;

Stadelmann, C .

NEUROLOGICAL SCIENCES, 2003, 24 (Suppl 5) :S265-S267

[3] Feedback inhibition of macrophage tumor necrosis factor-α production by tristetraprolin [J].

Carballo, E ;

Lai, WS ;

Blackshear, PJ .

SCIENCE, 1998, 281 (5379) :1001-1005

[4] ENDOTOXIN-INDUCED SERUM FACTOR THAT CAUSES NECROSIS OF TUMORS [J].

CARSWELL, EA ;

OLD, LJ ;

KASSEL, RL ;

GREEN, S ;

FIORE, N ;

WILLIAMSON, B .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1975, 72 (09) :3666-3670

[5] NF-κB and TNF-α:: A positive autocrine loop in human lung mast cells? [J].

Coward, WR ;

Okayama, Y ;

Sagara, H ;

Wilson, SJ ;

Holgate, ST ;

Church, MK .

JOURNAL OF IMMUNOLOGY, 2002, 169 (09) :5287-5293

[6]

Eugster HP, 1999, EUR J IMMUNOL, V29, P626, DOI 10.1002/(SICI)1521-4141(199902)29:02<626::AID-IMMU626>3.0.CO

[7]

2-A

[8] The application of multifactorial cluster analysis in the staging of plaques in early multiple sclerosis - Identification and characterization of the primary demyelinating lesion [J].

Gay, FW ;

Drye, TJ ;

Dick, GWA ;

Esiri, MM .

BRAIN, 1997, 120 :1461-1483

[9] Microglia as mediators of inflammatory and degenerative diseases [J].

González-Scarano, F ;

Baltuch, G .

ANNUAL REVIEW OF NEUROSCIENCE, 1999, 22 :219-240

[10] A tumour necrosis factor alpha autocrine loop contributes to proliferation and nuclear factor-κB activation of Theileria parva-transformed B cells [J].

Guergnon, J ;

Chaussepied, M ;

Sopp, P ;

Lizundia, R ;

Moreau, MF ;

Blumen, B ;

Werling, D ;

Howard, CJ ;

Langsley, G .

CELLULAR MICROBIOLOGY, 2003, 5 (10) :709-716

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