| First Author | Tailor P | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 1 | Pages | 243-55 |
| PubMed ID | 18566390 | Mgi Jnum | J:137177 |
| Mgi Id | MGI:3798146 | Doi | 10.4049/jimmunol.181.1.243 |
| Citation | Tailor P, et al. (2008) The proline-rich sequence of CD3epsilon as an amplifier of low-avidity TCR signaling. J Immunol 181(1):243-55 |
| abstractText | Engagement of peptide-MHC by the TCR induces a conformational change in CD3epsilon that exposes a proline-rich sequence (PRS) and recruits the cytoskeletal adaptor Nck. This event, which precedes phosphorylation of the CD3epsilon ITAM, has been implicated in synapse formation and T cell function. However, there is compelling evidence that responsiveness to TCR ligation is CD3epsilon PRS independent. In this study, we show that the CD3epsilon PRS is necessary for peptide-MHC-induced phosphorylation of CD3epsilon and for recruitment of protein kinase Ctheta to the immune synapse in differentiated CD8+ T lymphocytes. However, whereas these two events are dispensable for functional T cell responsiveness to high-avidity ligands, they are required for responsiveness to low-avidity ones. Thus, in at least certain T cell clonotypes, the CD3epsilon PRS amplifies weak TCR signals by promoting synapse formation and CD3epsilon phosphorylation. |
