An essential role for calmodulin in regulating human T cell aggregation

Susanna C. Fagerholm, Alan Prescott, Philip Cohen, Carl G. Gahmberg, Veli-Pekka Lehto (Editor)

    Research output: Contribution to journalArticle

    15 Citations (Scopus)

    Abstract

    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.
    Original languageEnglish
    Pages (from-to)131-6
    Number of pages6
    JournalFEBS Letters
    Volume491
    Issue number1-2
    DOIs
    Publication statusPublished - 28 Feb 2001

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