Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Publication Detail
Langerhans cells regulate cutaneous injury by licensing CD8 effector cells recruited to the skin.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Bennett CL, Fallah-Arani F, Conlan T, Trouillet C, Goold H, Chorro L, Flutter B, Means TK, Geissmann F, Chakraverty R
  • Publication date:
  • Pagination:
    7063, 7069
  • Journal:
  • Volume:
  • Issue:
  • Status:
  • Country:
    United States
  • PII:
  • Language:
  • Keywords:
    Aminoquinolines, Animals, Cell Communication, Cells, Cultured, Chimera, Cytotoxicity, Immunologic, Epidermis, Gene Expression Regulation, Graft vs Host Disease, Granzymes, Imiquimod, Interferon-gamma, Langerhans Cells, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, RNA, Messenger, T-Lymphocytes, Cytotoxic, TNF-Related Apoptosis-Inducing Ligand, Toll-Like Receptors, Tumor Necrosis Factor-alpha
Langerhans cells (LCs) are a distinct population of dendritic cells that form a contiguous network in the epidermis of the skin. Although LCs possess many of the properties of highly proficient dendritic cells, recent studies have indicated that they are not necessary to initiate cutaneous immunity. In this study, we used a tractable model of cutaneous GVHD, induced by topical application of a Toll-like receptor agonist, to explore the role of LCs in the development of tissue injury. By adapting this model to permit inducible and selective depletion of host LCs, we found that GVHD was significantly reduced when LCs were absent. However, LCs were not required either for CD8 T-cell activation within the draining lymph node or subsequent homing of effector cells to the epidermis. Instead, we found that LCs were necessary for inducing transcription of IFN-γ and other key effector molecules by donor CD8 cells in the epidermis, indicating that they license CD8 cells to induce epithelial injury. These data demonstrate a novel regulatory role for epidermal LCs during the effector phase of an inflammatory immune response in the skin.
Publication data is maintained in RPS. Visit https://rps.ucl.ac.uk
 More search options
UCL Researchers
Research Department of Haematology
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by