| Literature DB >> 17676044 |
Nicholas J Wilson1, Katia Boniface, Jason R Chan, Brent S McKenzie, Wendy M Blumenschein, Jeanine D Mattson, Beth Basham, Kathleen Smith, Taiying Chen, Franck Morel, Jean-Claude Lecron, Robert A Kastelein, Daniel J Cua, Terrill K McClanahan, Edward P Bowman, Rene de Waal Malefyt.
Abstract
T(H)-17 cells are a distinct lineage of proinflammatory T helper cells that are essential for autoimmune disease. In mice, commitment to the T(H)-17 lineage is dependent on transforming growth factor-beta and interleukin 6 (IL-6). Here we demonstrate that IL-23 and IL-1beta induced the development of human T(H)-17 cells expressing IL-17A, IL-17F, IL-22, IL-26, interferon-gamma, the chemokine CCL20 and transcription factor RORgammat. In situ, T(H)-17 cells were identified by expression of the IL-23 receptor and the memory T cell marker CD45RO. Psoriatic skin lesions contained IL-23-producing dendritic cells and were enriched in the cytokines produced by human T(H)-17 cells that promote the production of antimicrobial peptides in human keratinocytes. Our data collectively indicate that human and mouse T(H)-17 cells require distinct factors during differentiation and that human T(H)-17 cells may regulate innate immunity in epithelial cells.Entities:
Mesh:
Substances:
Year: 2007 PMID: 17676044 DOI: 10.1038/ni1497
Source DB: PubMed Journal: Nat Immunol ISSN: 1529-2908 Impact factor: 25.606