Recombinant glucocorticoid induced tumor necrosis factor receptor (rGITR) induces NOS in murine macrophage

被引:47
作者
Shin, HH
Lee, MH
Kim, SG
Lee, YH
Kwon, BS
Choi, HS [1 ]
机构
[1] Univ Ulsan, Dept Biol Sci, Ulsan 680749, South Korea
[2] Univ Ulsan, Immunomodulat Res Ctr, Ulsan 680749, South Korea
关键词
glucocorticoid induced tumor necrosis factor; receptor; inducible nitric oxide synthase; macrophage; nitric oxide;
D O I
10.1016/S0014-5793(02)02379-7
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
Glucocorticoid induced tumor necrosis factor receptor (GITR) is a new member of the tumor necrosis factor-nerve growth factor receptor superfamily of which the function has not been well studied. The extracellular domain of GITR was produced in Escherichia coli and purified as a single band of predicted M-r of 18.0 kDa. GITR and GITR ligand were expressed constitutively on the surface of Raw 264.7 macrophage cell line and murine peritoneal macrophages. An extracellular domain of GITR can activate murine macrophages to express inducible nitric oxide synthase and to generate nitric oxide in a dose- and time-dependent manner. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:275 / 280
页数:6
相关论文
共 29 条
[1]   4-1BB and Ox40 are members of a tumor necrosis factor (TNF)-nerve growth factor receptor subfamily that bind TNF receptor-associated factors and activate nuclear factor κB [J].
Arch, RH ;
Thompson, CB .
MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (01) :558-565
[2]   An essential regulatory role for macrophage migration inhibitory factor in T-cell activation [J].
Bacher, M ;
Metz, CN ;
Calandra, T ;
Mayer, K ;
Chesney, J ;
Lohoff, M ;
Gemsa, D ;
Donnelly, T ;
Bucala, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (15) :7849-7854
[3]  
CALEDA A, 1994, IMMUNOL TODAY, V15, P100
[4]  
CAMERINI D, 1991, J IMMUNOL, V147, P3165
[5]   Inhibition of caspase 3 abrogates lipopolysaccharide-induced nitric oxide production by preventing activation of NF-κB and c-Jun NH2-terminal kinase/stress-activated protein kinase in RAW 264.7 murine macrophage cells [J].
Chakravortty, D ;
Kato, Y ;
Sugiyama, T ;
Koide, N ;
Mu, MM ;
Yoshida, T ;
Yokochi, T .
INFECTION AND IMMUNITY, 2001, 69 (03) :1315-1321
[6]   Potential role of the JNK/SAPK signal transduction pathway in the induction of iNOS by TNF-α [J].
Chan, ED ;
Riches, DWH .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 253 (03) :790-796
[7]  
Chan ED, 1999, J IMMUNOL, V162, P415
[8]   Pole of the cyclic AMP-protein kinase a pathway in lipopolysaccharide-induced nitric oxide synthase expression in RAW 264.7 macrophages - Involvement of cyclooxygenase-2 [J].
Chen, CC ;
Chiu, KT ;
Sun, YT ;
Chen, WC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (44) :31559-31564
[9]   Induction of cell death by tumour necrosis factor (TNF) receptor 2, CD40 and CD30:: a role for TNF-R1 activation by endogenous membrane-anchored TNF [J].
Grell, M ;
Zimmermann, G ;
Gottfried, E ;
Chen, CM ;
Grünwald, U ;
Huang, DCS ;
Lee, YHW ;
Dürkop, H ;
Engelmann, H ;
Scheurich, P ;
Wajant, H ;
Strasser, A .
EMBO JOURNAL, 1999, 18 (11) :3034-3043
[10]  
Heinisch IVWM, 2000, EUR J IMMUNOL, V30, P3441, DOI 10.1002/1521-4141(2000012)30:12<3441::AID-IMMU3441>3.0.CO