REGULATION OF T-CELL PROLIFERATION BY ANTI-CD49D AND ANTI-CD29 MONOCLONAL-ANTIBODIES

被引:22
作者
BEDNARCZYK, JL
TEAGUE, TK
WYGANT, JN
DAVIS, LS
LIPSKY, PE
MCINTYRE, BW
机构
[1] UNIV TEXAS,SW MED CTR,HAROLD C SIMMONS ARTHRITIS RES CTR,DALLAS,TX 75230
[2] UNIV TEXAS,SW MED CTR,DEPT INTERNAL MED,DALLAS,TX 75230
关键词
VLA-4; INTEGRINS; CD49D; CD29;
D O I
10.1002/jlb.52.4.456
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The beta1 integrin VLA-4 (alpha4beta1, CD49d/CD29), which is expressed on a large subpopulation of peripheral blood T lymphocytes, functions as a receptor for the endothelial adhesion protein VCAM-1 and the extracellular matrix protein fibronectin. Previous studies showed that immobilized fibronectin enhanced anti-CD3 monoclonal antibody (mAb)-induced T cell proliferation through binding to the integrins VLA-4 and VLA-5 (alpha5beta1, CD49e/CD29). We studied the ability of the anti-CD49d mAb L25 to potentiate proliferation. T cell proliferation was induced by subthreshold concentrations of anti-CD3 mAb (mAb OKT3) coimmobilized with mAb L25 but not with coimmobilized anti-CD29 (beta1) mAb. Soluble anti-CD29 mAb inhibited the proliferation induced by coimmobilized mAb OKT3 and L25 but not proliferation induced by mAb OKT3 with PMA or coimmobilized anti-CD26 mAb.
引用
收藏
页码:456 / 462
页数:7
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