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T cell receptor (TCR) microclusters form within seconds of T cell contact with supported planar bilayers containing intercellular adhesion molecule-1 and agonist major histocompatibility complex (MHC)-peptide complexes, and elevation of cytoplasmic Ca2+ is observed within seconds of the first detectable microclusters. At 0-30 s after contact, TCR microclusters are colocalized with activated forms of Lck, ZAP-70, and the linker for activation of T cells. By 2 min, activated kinases are reduced in the older central microclusters, but are abundant in younger peripheral microclusters. By 5 min, TCR in the central supramolecular activation cluster have reduced activated kinases, whereas faint peripheral TCR microclusters efficiently generated activated Lck and ZAP-70. TCR microcluster formation is resistant to inhibition by Src family kinase inhibitor PP2, but is abrogated by actin polymerization inhibitor latrunculin A. We propose that Src kinase-independent formation of TCR microclusters in response to agonist MHC-peptide provides an actin-dependent scaffold for signal amplification.

Original publication

DOI

10.1084/jem.20051182

Type

Journal article

Journal

The Journal of experimental medicine

Publication Date

10/10/2005

Volume

202

Pages

1031 - 1036

Addresses

Department of Pathology and the Program in Molecular Pathogenesis, Skirball Institute of Biomolecular Medicine, New York, NY 10016, USA.

Keywords

T-Lymphocytes, Cells, Cultured, Animals, Mice, Transgenic, Mice, Calcium, Actins, Intercellular Adhesion Molecule-1, Receptors, Antigen, T-Cell, Signal Transduction, Major Histocompatibility Complex, Time Factors