Cutting edge: dendritic epidermal γδ T cell ligands are rapidly and locally expressed by keratinocytes following cutaneous wounding

• Published in: The Journal of immunology (1950) 2012-04, Vol.188 (7), p.2972-2976
• Main Authors: Komori, H Kiyomi, Witherden, Deborah A, Kelly, Ryan, Sendaydiego, Kevin, Jameson, Julie M, Teyton, Luc, Havran, Wendy L
• Format: Article
• Language: English
• Subjects: Animals; Gene Expression Regulation; Keratinocytes - metabolism; Langerhans Cells - immunology; Ligands; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, Antigen, T-Cell, gamma-delta - deficiency; Receptors, Antigen, T-Cell, gamma-delta - genetics; Receptors, Antigen, T-Cell, gamma-delta - immunology; T-Lymphocyte Subsets - immunology; Thymus Gland - embryology; Thymus Gland - immunology; Wound Healing - immunology
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.1100887

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.