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We investigated the role of the T cell antigen receptor (TcR) in control of T cell migration in an in vitro system. We used T cells from transgenic mice bearing a TcR for the lysozyme peptide 48-62 bound to I-A(k) (3A9). T cells from the 3A9 TcR transgenic mice crawled on purified intercellular adhesion molecule-1 substrates, but strikingly, stopped upon interaction with the physiological ligand, i.e., the mouse I-A(k) with covalently attached hen egg white lysozyme peptide residues 48-62 complex. TcR-triggered stopping was reversible by treatment with adhesion-strengthening phorbol esters. The microtubule organizing center of stopped cells was positioned adjacent to the site of stable cell anchorage. Direct conversion of lymphocyte function associated-1 to the high-affinity conformation with antibodies also stopped T cells in a similar manner to antigen. Thus, physiological TcR engagement triggers a stop signal through lymphocyte function associated-1. We propose that the stop signal is an early and essential event in T cell activation that also will play an important role in control of T cell migration.

Type

Journal article

Journal

Proceedings of the National Academy of Sciences of the United States of America

Publication Date

04/1997

Volume

94

Pages

3909 - 3913

Addresses

Center for Immunology and Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA. dustin@pathbox.wustl.edu

Keywords

T-Lymphocytes, Animals, Mice, Transgenic, Mice, Receptors, Antigen, T-Cell, Signal Transduction, Cell Movement