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Visualizing the Dynamics of T Cell Activation: Intracellular Adhesion Molecule 1 Migrates Rapidly to the T Cell/B Cell Interface and Acts to Sustain Calcium Levels

Christoph Wulfing, Michael D. Sjaastad and Mark M. Davis
Proceedings of the National Academy of Sciences of the United States of America
Vol. 95, No. 11 (May 26, 1998), pp. 6302-6307
Stable URL: http://www.jstor.org/stable/45374
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Visualizing the Dynamics of T Cell Activation: Intracellular Adhesion Molecule 1 Migrates Rapidly to the T Cell/B Cell Interface and Acts to Sustain Calcium Levels
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Abstract

T cell recognition typically involves both the engagement of a specific T cell receptor with a peptide/major histocompatibility complex (MHC) and a number of accessory interactions. One of the most important interactions is between the integrin lymphocyte function-associated antigen 1 (LFA-1) on the T cell and intracellular adhesion molecule 1 (ICAM-1) on an antigen-presenting cell. By using fluorescence video microscopy and an ICAM-1 fused to a green fluorescent protein, we find that the elevation of intracellular calcium in the T cell that is characteristic of activation is followed almost immediately by the rapid accumulation of ICAM-1 on a B cell at a tight interface between the two cells. This increased density of ICAM-1 correlates with the sustained elevation of intracellular calcium in the T cell, known to be critical for activation. The use of peptide/MHC complexes and ICAM-1 on a supported lipid bilayer to stimulate T cells also indicates a major role for ICAM-1/LFA-1 in T cell activation but, surprisingly, not for adhesion, as even in the absence of ICAM-1 the morphological changes and adhesive characteristics of an activated T cell are seen in this system. We suggest that T cell antigen receptor-mediated recognition of a very small number of MHC/peptide complexes could trigger LFA-1/ICAM-1 clustering and avidity regulation, thus amplifying and stabilizing the production of second messengers.

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