| First Author | Liu SD | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 9 | Pages | 5283-95 |
| PubMed ID | 19380775 | Mgi Jnum | J:147951 |
| Mgi Id | MGI:3843087 | Doi | 10.4049/jimmunol.0803811 |
| Citation | Liu SD, et al. (2009) Galectin-1 tunes TCR binding and signal transduction to regulate CD8 burst size. J Immunol 182(9):5283-95 |
| abstractText | 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. |
