Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
J Immunol. 2012 Apr 1;188(7):2972-6. doi: 10.4049/jimmunol.1100887. Epub 2012 Mar 5.
TCR-specific activation is pivotal to dendritic epidermal T cell (DETC) function during cutaneous wound repair. However, DETC TCR ligands are uncharacterized, and little is known about their expression patterns and kinetics. Using soluble DETC TCR tetramers, we demonstrate that DETC TCR ligands are not constitutively expressed in healthy tissue but are rapidly upregulated following wounding on keratinocytes bordering wound edges. Ligand expression is tightly regulated, with downmodulation following DETC activation. Early inhibition of TCR-ligand interactions using DETC TCR tetramers delays wound repair in vivo, highlighting DETC as rapid responders to injury. To our knowledge, this is the first visualization of DETC TCR ligand expression, which provides novel information about how ligand expression impacts early stages of DETC activation and wound repair.
T 细胞受体（TCR）特异性激活对于皮肤创伤修复过程中树突状表皮 T 细胞（DETC）的功能至关重要。然而，DETC TCR 的配体尚未被阐明，其表达模式和动力学也知之甚少。通过可溶性 DETC TCR 四聚体，我们证明 DETC TCR 配体在健康组织中不是组成性表达的，而是在伤口边缘的角质形成细胞上发生创伤后迅速上调。配体表达受到严格调控，随着 DETC 的激活，配体表达下调。早期使用 DETC TCR 四聚体抑制 TCR-配体相互作用会延迟体内伤口愈合，这突出了 DETC 是对损伤的快速反应细胞。据我们所知，这是首次可视化 DETC TCR 配体表达，为配体表达如何影响 DETC 早期激活和伤口修复提供了新的信息。
