| Literature DB >> 20130970 |
Satoshi Itoh1, Susumu Nakae, Robert C Axtell, Jeffrey B Velotta, Naoyuki Kimura, Naoki Kajiwara, Yoichiro Iwakura, Hirohisa Saito, Hideo Adachi, Lawrence Steinman, Robert C Robbins, Michael P Fischbein.
Abstract
BACKGROUND: Although interleukin-17 (IL-17) has been reported to participate in the pathogenesis of infectious, autoimmune and allergic disorders, the precise role in allograft rejection remains uncertain. This study illustrates that IL-17 contributes to the pathogenesis of chronic allograft rejection. RESULT: Utilizing a murine heterotopic heart transplant model system, IL-17-deficient recipient mice had decreased allograft inflammatory cell recruitment, decreased IL-6, MCP-1, and KC production, and reduced graft coronary artery disease (GCAD). Intragraft gamma delta (gammadelta) T cells appear to be the predominant source of IL-17 production.Entities:
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Year: 2010 PMID: 20130970 DOI: 10.1007/s10875-009-9366-9
Source DB: PubMed Journal: J Clin Immunol ISSN: 0271-9142 Impact factor: 8.317