Journal
JOURNAL OF CLINICAL IMMUNOLOGY
Volume 30, Issue 2, Pages 235-240Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10875-009-9366-9
Keywords
IL-17; graft coronary artery disease; gamma delta T cell
Categories
Funding
- Falk Research Fund, Department of Cardiothoracic Surgery at Stanford University Medical School, American Association for Thoracic Surgery
- National Institute of Biomedical Innovation [ID 05-24]
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT) [20790700]
- Program for Improvement of Research Environment for Young Researchers
- Grants-in-Aid for Scientific Research [20790700] Funding Source: KAKEN
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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. 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 (gamma delta) T cells appear to be the predominant source of IL-17 production. Therefore, IL-17 neutralization may provide a potential target for novel therapeutic treatment for cardiac allograft rejection.
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