References
Query Results -- Details
MGI Accession ID: MGI:3843087
J Number: J:147951
Other Accession IDs:
Title: Galectin-1 tunes TCR binding and signal transduction to regulate CD8 burst size.
Authors: Liu SD; Tomassian T; Bruhn KW; Miller JF; Poirier F; Miceli MC
Journal: J Immunol
Volume: 182
Issue: 9
Date: 2009 May 1
Year: 2009
Pages: 5283-95
Review Status: Peer Reviewed
Abstract:
T cell burst size is regulated by the duration of TCR engagement and balanced control of Ag-induced activation, expansion, and apoptosis. We found that galectin-1-deficient CD8 T cells undergo greater cell division in response to TCR stimulation, with fewer dividing cells undergoing apoptosis. TCR-induced ERK signaling was sustained in activated galectin-1-deficient CD8 T cells and antagonized by recombinant galectin-1, indicating galectin-1 modulates TCR feed-forward/feedback loops involved in signal discrimination and procession. Furthermore, recombinant galectin-1 antagonized binding of agonist tetramers to the TCR on activated OT-1 T cells. Finally, galectin-1 produced by activated Ag-specific CD8 T cells negatively regulated burst size and TCR avidity in vivo. Therefore, galectin-1, inducibly expressed by activated CD8 T cells, functions as an autocrine negative regulator of peripheral CD8 T cell TCR binding, signal transduction, and burst size. Together with recent findings demonstrating that gal-1 promotes binding of agonist tetramers to the TCR of OT-1 thymocytes, these studies identify galectin-1 as a tuner of TCR binding, signaling, and functional fate determination that can differentially specify outcome, depending on the developmental and activation stage of the T cell.
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