Membrane-targeted complement inhibitors

被引：63

作者：

Smith, GP ^{[1
]}

Smith, RAG ^{[1
]}

机构：

[1] Adprotech, Saffron Walden CB10 1XL, Essex, England

来源：

MOLECULAR IMMUNOLOGY | 2001年 / 38卷 / 2-3期

关键词：

cell membrane; human disease; cytolytic pore;

D O I：

10.1016/S0161-5890(01)00047-5

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：

Undesirable complement activation contributes to the pathology of many human diseases by damaging tissue and promoting inflammation. Because complement-mediated damage is caused by the deposition of complement components on the cell surface, several strategies have been devised to target complement regulator proteins to cell membranes. These strategies have resulted in engineered proteins that have improved potency in vitro and enhanced therapeutic benefit in animal models of disease. One membrane-targeted complement inhibitor has now entered clinical development and this class of second-generation agents may provide effective therapies for the treatment of a variety of disease states. (C) 2001 Elsevier Science Ltd. All rights reserved.

引用

收藏

页码：249 / 255

页数：7

相关论文

共 48 条

[1] STRUCTURE AND FUNCTION OF THE COMPLEMENT RECEPTORS, CR-1 (CD35) AND CR-2 (CD21) [J].

AHEARN, JM ;

FEARON, DT .

ADVANCES IN IMMUNOLOGY, 1989, 46 :183-219

[2] ENDOTHELIAL-LEUKOCYTE ADHESION MOLECULES IN HUMAN-DISEASE [J].

BEVILACQUA, MP ;

NELSON, RM ;

MANNORI, G ;

CECCONI, O .

ANNUAL REVIEW OF MEDICINE, 1994, 45 :361-378

[3] SIALYL LEWIS(X)-CONTAINING OLIGOSACCHARIDE ATTENUATES MYOCARDIAL REPERFUSION INJURY IN CATS [J].

BUERKE, M ;

WEYRICH, AS ;

ZHENG, ZL ;

GAETA, FCA ;

FORREST, MJ ;

LEFER, AM .

JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (03) :1140-1148

[4] IMMUNOCYTOCHEMICAL LOCALIZATION OF THE TERMINAL COMPLEMENT COMPLEX IN MULTIPLE-SCLEROSIS [J].

COMPSTON, DAS ;

MORGAN, BP ;

CAMPBELL, AK ;

WILKINS, P ;

COLE, G ;

THOMAS, ND ;

JASANI, B .

NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1989, 15 (04) :307-316

[5] CD59, AN LY-6-LIKE PROTEIN EXPRESSED IN HUMAN LYMPHOID-CELLS, REGULATES THE ACTION OF THE COMPLEMENT MEMBRANE ATTACK COMPLEX ON HOMOLOGOUS CELLS [J].

DAVIES, A ;

SIMMONS, DL ;

HALE, G ;

HARRISON, RA ;

TIGHE, H ;

LACHMANN, PJ ;

WALDMANN, H .

JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 170 (03) :637-654

[6] RELEASE OF DECAY-ACCELERATING FACTOR (DAF) FROM THE CELL-MEMBRANE BY PHOSPHATIDYLINOSITOL-SPECIFIC PHOSPHOLIPASE-C (PIPLC) - SELECTIVE MODIFICATION OF A COMPLEMENT REGULATORY PROTEIN [J].

DAVITZ, MA ;

LOW, MG ;

NUSSENZWEIG, V .

JOURNAL OF EXPERIMENTAL MEDICINE, 1986, 163 (05) :1150-1161

[7] Overexpression in Escherichia coli, folding, purification, and characterization of the first three short consensus repeat modules of human complement receptor type 1 [J].

Dodd, I ;

Mossakowska, DE ;

Camilleri, P ;

Haran, M ;

Hensley, P ;

Lawlor, EJ ;

McBay, DL ;

Pindar, W ;

Smith, RAG .

PROTEIN EXPRESSION AND PURIFICATION, 1995, 6 (06) :727-736

[8]

DODD L, 2000, IMMUNOPHARMACOLOGY, V49, P63

[9] Strategies for targeting complement inhibitors in ischaemia/reperfusion injury [J].

Dong, J ;

Pratt, JR ;

Smith, RAG ;

Dodd, I ;

Sacks, SH .

MOLECULAR IMMUNOLOGY, 1999, 36 (13-14) :957-963

[10] IDENTIFICATION OF THE MEMBRANE GLYCOPROTEIN THAT IS THE C3B RECEPTOR OF THE HUMAN-ERYTHROCYTE, POLYMORPHONUCLEAR LEUKOCYTE, LYMPHOCYTE-B, AND MONOCYTE [J].

FEARON, DT .

JOURNAL OF EXPERIMENTAL MEDICINE, 1980, 152 (01) :20-30

← 1 2 3 4 5 →