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摘要
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 gamma delta T cells and their fetal thymic TCR gamma delta precursors, and it is the most abundantly expressed member on intestinal intraepithelial gamma delta T cell lymphocytes. In this study, we provide mechanistic insights into the regulation of Ly49e expression in gamma delta T cells. First, we demonstrate that TCR-mediated activation of intraepithelial gamma delta 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 gamma delta T cell subsets, whereas it is not observed in spleen gamma delta T cells. By investigating Ly49e promoter activities and lymphotoxin (LT) alpha beta dependency in resting versus TCR-activated intraepithelial gamma delta T cells, we reveal two separate regulatory pathways for Ly49E expression, as follows: a LT alpha beta-dependent pathway leading to basal Ly49E expression in resting cells that is induced by Pro2-mediated Ly49e transcription, and a LT alpha beta-independent pathway leading to elevated, Pro3-driven Ly49E expression in TCR-stimulated cells. The Journal of Immunology, 2013, 190: 1982-1990.
- 出版日期2013-3-1
