The immunological synapse and CD28-CD80 interactions

被引：233

作者：

Bromley, SK

Iaboni, A

Davis, SJ

Whitty, A

Green, JM

Shaw, AS

Weiss, A

Dustin, ML ^{[1
]}

机构：

[1] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Med, Div Rheumatol, San Francisco, CA 94143 USA

[2] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA

[3] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA

[4] Univ Oxford, Nuffield Dept Med, Oxford, England

[5] Biogen Inc, Cambridge, MA 02142 USA

[6] NYU, Sch Med, Dept Pathol, New York, NY USA

[7] NYU, Sch Med, Program Mol Pathogenesis, New York, NY USA

[8] Skirball Inst Biomol Med, New York, NY USA

来源：

NATURE IMMUNOLOGY | 2001年 / 2卷 / 12期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1038/ni737

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

According to the two-signal model of T cell activation, costimulatory molecules augment T cell receptor (TCR) signaling, whereas adhesion molecules enhance TCR-MHC-peptide recognition. The structure and binding properties of CD28 imply that it may perform both functions, blurring the distinction between adhesion and costimulatory molecules. Our results show that CD28 on naive T cells does not support adhesion and has little or no capacity for directly enhancing TCR-MHC-peptide interactions. Instead of being dependent on costimulatory signaling, we propose that a key function of the immunological synapse is to generate a cellular microenvironment that favors the interactions of potent secondary signaling molecules, such as CD28.

引用

页码：1159 / 1166

页数：8

共 60 条

[1] CD28 IS ASSOCIATED WITH AND INDUCES THE IMMEDIATE TYROSINE PHOSPHORYLATION AND ACTIVATION OF THE TEC FAMILY KINASE ITK/EMT IN THE HUMAN JURKAT LEUKEMIC T-CELL LINE [J].