| First Author | Van Den Broeck T | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 5 | Pages | 1982-90 |
| PubMed ID | 23338239 | Mgi Jnum | J:193490 |
| Mgi Id | MGI:5468614 | Doi | 10.4049/jimmunol.1200354 |
| Citation | Van Den Broeck T, et al. (2013) Differential Ly49e Expression Pathways in Resting versus TCR-Activated Intraepithelial gammadelta T Cells. J Immunol 190(5):1982-90 |
| abstractText | The Ly49 NK receptor family in mice is composed of several members that recognize MHC class I (MHC-I) or MHC-I-related molecules. We and others have shown before that Ly49E is a unique member, with a different expression pattern on NK cells and being triggered by the non-MHC-I-related protein urokinase plasminogen activator. Among the entire Ly49 receptor family, Ly49E is the only Ly49 member expressed by epidermal-localized gammadelta T cells and their fetal thymic TCRgammadelta precursors, and it is the most abundantly expressed member on intestinal intraepithelial gammadelta T cell lymphocytes. In this study, we provide mechanistic insights into the regulation of Ly49e expression in gammadelta T cells. First, we demonstrate that TCR-mediated activation of intraepithelial gammadelta T cells significantly increases Ly49E expression. This results from de novo Ly49E expression and is highly selective, because no other Ly49 family members are induced. TCR-mediated Ly49E induction is a conserved feature of skin- and gut-residing intraepithelial-localized gammadelta T cell subsets, whereas it is not observed in spleen gammadelta T cells. By investigating Ly49e promoter activities and lymphotoxin (LT) alphabeta dependency in resting versus TCR-activated intraepithelial gammadelta T cells, we reveal two separate regulatory pathways for Ly49E expression, as follows: a LTalphabeta-dependent pathway leading to basal Ly49E expression in resting cells that is induced by Pro2-mediated Ly49e transcription, and a LTalphabeta-independent pathway leading to elevated, Pro3-driven Ly49E expression in TCR-stimulated cells. |
