An essential role for calmodulin in regulating human T cell aggregation

FEBS Letters

Fagerholm, Susanna C.¹  Prescott, Alan²  Gahmberg, Carl G.³  Cohen, Philip¹ 

[1] Medical Research Council Protein Phosphorylation Unit, University of Dundee, Dundee, UK;School of Life Sciences, University of Dundee, Dundee, UK;Division of Biochemistry, Department of Biosciences, University of Helsinki, Helsinki, Finland

关键词: T lymphocyte;    Adhesion;    Calmodulin;    Integrin;    Cytoskeleton;    ICAM;    intercellular adhesion molecule;    PI 3-kinase;    phosphatidylinositide 3-OH kinase;    PDBu;    phorbol 12;    13-dibutyrate;    MLC;    myosin light chain;    mTOR;    mammalian target of rapamycin;    CsA;    cyclosporin;    CaMKII;    calcium-calmodulin-dependent kinase II;    NFAT;    nuclear factor for activated T cells;   

DOI  :  10.1016/S0014-5793(01)02182-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

After activation of T cells with either CD3 antibodies or phorbol esters, we have found that T cell–cell aggregation, integrin-dependent actin reorganisation and cell spreading are strongly suppressed by any of three structurally different calmodulin antagonists, without any effect on the amount of CD11/CD18 integrin binding to the actin cytoskeleton. However, only T cell receptor-induced, and not phorbol ester-induced, aggregation and cell spreading are prevented by inhibitors of phosphatidylinositide (PI) 3-kinase. These results suggest that PI 3-kinase lies upstream of calmodulin in the signalling pathway leading to T cell aggregation, cell spreading and actin reorganisation and that cell spreading and actin reorganisation are essential for T cell adhesion.

【 授权许可】

Unknown