The regulation of the complement system: insights from genetically-engineered mice

被引：44

作者：

Turnberg, D ^{[1
]}

Botto, M ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Div Med, Rheumatol Sect, London W12 0NN, England

来源：

MOLECULAR IMMUNOLOGY | 2003年 / 40卷 / 2-4期

关键词：

complement; complement regulatory proteins; genetically modified mice;

D O I：

10.1016/S0161-5890(03)00110-X

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：

The complement system is very tightly regulated by fluid-phase and membrane-bound factors that prevent injury to self-tissues. The study of genetically engineered animals with targeted deletion or gain of function mutations has highlighted the important role that many of the complement inhibitors play in vivo. The advantages and disadvantages of this type of approach are discussed and the insights gained from the investigation of these animals are reviewed. (C) 2003 Elsevier Ltd. All rights reserved.

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收藏

页码：145 / 153

页数：9

相关论文

共 107 条

[11]

Bürger A, 1999, EUR J IMMUNOL, V29, P1188, DOI 10.1002/(SICI)1521-4141(199904)29:04<1188::AID-IMMU1188>3.0.CO

[12]

2-F

[13] PROTECTION OF XENOGENEIC CARDIAC ENDOTHELIUM FROM HUMAN-COMPLEMENT BY EXPRESSION OF CD59 OR DAF IN TRANSGENIC MICE [J].

BYRNE, GW ;

MCCURRY, KR ;

KAGAN, D ;

QUINN, C ;

MARTIN, MJ ;

PLATT, JL ;

LOGAN, JS .

TRANSPLANTATION, 1995, 60 (10) :1149-1156

[14] CLONING OF DECAY-ACCELERATING FACTOR SUGGESTS NOVEL USE OF SPLICING TO GENERATE 2 PROTEINS [J].

CARAS, IW ;

DAVITZ, MA ;

RHEE, L ;

WEDDELL, G ;

MARTIN, DW ;

NUSSENZWEIG, V .

NATURE, 1987, 325 (6104) :545-549

[15]

Chen GT, 2001, ARS COMBINATORIA, V59, P33

[16] Comparative analysis of three genetic modifications designed to inhibit human serum-mediated cytolysis [J].

Costa, C ;

Zhao, L ;

Decesare, S ;

Fodor, WL .

XENOTRANSPLANTATION, 1999, 6 (01) :6-16

[17] Complement (C5b-9) induces DNA synthesis in rat mesangial cells in vitro [J].

Couser, WG ;

Pippin, JW ;

Shankland, SJ .

KIDNEY INTERNATIONAL, 2001, 59 (03) :905-912

[18] High-level endothelial expression of human CD59 prolongs heart function in an ex vivo model of xenograft rejection [J].

Cowan, PJ ;

Somerville, CA ;

Shinkel, TA ;

Katerelos, M ;

Aminian, A ;

Romanella, M ;

Tange, MJ ;

Pearse, MJ ;

D'Apice, AJF .

TRANSPLANTATION, 1998, 65 (06) :826-831

[19] Knock out of α1,3-galactosyltransferase or expression of α1,2-fucosyltransferase further protects CD55- and CD59-expressing mouse hearts in an ex vivo model of xenograft rejection [J].

Cowan, PJ ;

Chen, CG ;

Shinkel, TA ;

Fisicaro, N ;

Salvaris, E ;

Aminian, A ;

Romanella, M ;

Pearse, MJ ;

D'Apice, AJF .

TRANSPLANTATION, 1998, 65 (12) :1599-1604

[20] High-level co-expression of complement regulators on vascular endothelium in transgenic mice: CD55 and CD59 provide greater protection from human complement-mediated injury than CD59 alone [J].

Cowan, PJ ;

Shinkel, TA ;

Aminian, A ;

Romanella, M ;

Wigley, PL ;

Lonie, AJ ;

Nottle, MB ;

Pearse, MJ ;

d'Apice, AJF .

XENOTRANSPLANTATION, 1998, 5 (03) :184-190

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