HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Whang, M. I. Articles by Raulet, D. H. Search for Related Content PubMed PubMed Citation Articles by Whang, M. I. Articles by Raulet, D. H.

Costimulation of Dendritic Epidermal T Cells by a New NKG2D Ligand Expressed Specifically in the Skin ¹

Department of Molecular and Cell Biology and Cancer Research Laboratory, University of California, Berkeley, CA 94720

Dendritic epidermal T cells (DETCs) are a highly specialized population of T cells that resides in the murine skin and participates in wound healing and tumor surveillance. Despite the expression of other stimulatory receptors on these cells, mechanisms involving activation have focused primarily on the invariant V3-V1 TCR expressed by DETCs. All DETCs also express the activating NKG2D receptor, but the role of NKG2D in DETC activation remains unclear, as does the identity of NKG2D ligands that are functionally expressed in the skin. In this study, we document the cloning of an NKG2D ligand H60c that is expressed specifically in the skin and in cultured keratinocytes and demonstrate its role in the activation of DETCs and NK cells. The ligand is unique among NKG2D ligands in being up-regulated in cultured keratinocytes, and its interaction with NKG2D is essential for DETC activation. Importantly, it is shown that engagement of NKG2D is not sufficient to activate DETCs, but instead provides a costimulatory signal that is nevertheless essential for activating DETCs in response to stimulation with keratinocytes.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the National Institutes of Health (to D.H.R.).

² Address correspondence and reprint requests to Dr. David H. Raulet, Department of Molecular and Cell Biology, University of California, Berkeley, 142 Life Sciences Addition 3200, Berkeley, CA 94720-3200. E-mail address: raulet{at}berkeley.edu

³ Abbreviations used in this paper: DETC, dendritic epidermal T cell; Mult1, murine UL-16-binding protein-like transcript 1; Rae1, retinoic acid early inducible 1; H60/60a/60c, Histocompatibility 60/60a/60c;ORF, open reading frame; For, forward; Rev, reverse; ULBP, UL-16 binding protein.