LONG-TERM SURVIVAL OF XENOGENEIC PANCREATIC-ISLET GRAFTS INDUCED BY CTLA4IG

被引：1144
|
作者：
LENSCHOW, DJ
ZENG, YJ
THISTLETHWAITE, JR
MONTAG, A
BRADY, W
GIBSON, MG
LINSLEY, PS
BLUESTONE, JA
机构：
[1] UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637
[2] UNIV CHICAGO,COMM IMMUNOL,CHICAGO,IL 60637
[3] UNIV CHICAGO,DEPT SURG,CHICAGO,IL 60637
[4] UNIV CHICAGO,DEPT PATHOL,CHICAGO,IL 60637
[5] BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121
来源：
SCIENCE | 1992年 / 257卷 / 5071期
关键词：
D O I：
10.1126/science.1323143
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Antigen-specific T cell activation depends on T cell receptor-ligand interaction and co-stimulatory signals generated when accessory molecules bind to their ligands, such as CD28 to the B7 (also called BB1) molecule. A soluble fusion protein of human CTLA-4 (a protein homologous to CD28) and the immunoglobulin (Ig) G1 Fc region (CTLA4Ig) binds to human and murine B7 with high avidity and blocks T cell activation in vitro. CTLA4Ig therapy blocked human pancreatic islet rejection in mice by directly affecting T cell recognition of B7+ antigen-presenting cells. In addition, CTLA4Ig induced long-term, donor-specific tolerance, which may have applications to human organic transplantation.
引用
收藏
页码：789 / 792
页数：4
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