TY - JOUR
T1 - IL-17 contributes to the development of chronic rejection in a murine heart transplant model
AU - Itoh, Satoshi
AU - Nakae, Susumu
AU - Axtell, Robert C.
AU - Velotta, Jeffrey B.
AU - Kimura, Naoyuki
AU - Kajiwara, Naoki
AU - Iwakura, Yoichiro
AU - Saito, Hirohisa
AU - Adachi, Hideo
AU - Steinman, Lawrence
AU - Robbins, Robert C.
AU - Fischbein, Michael P.
N1 - Funding Information:
Acknowledgments This work was supported by funds from the Falk Research Fund, Department of Cardiothoracic Surgery at Stanford University Medical School, American Association for Thoracic Surgery (Norman E. Shumway award to MPF), National Institute of Biomedical Innovation (ID 05-24; H.S.), Ministry of Education, Culture, Sports, Science, and Technology (MEXT) (20790700: N.K.), and Program for Improvement of Research Environment for Young Researchers, The Special Coordination Funds for Promoting Science and Technology of MEXT (S.N.). The authors have no conflicting financial interests.
PY - 2010/3
Y1 - 2010/3
N2 - 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 (γδ) T cells appear to be the predominant source of IL-17 production. Conclusion Therefore, IL-17 neutralization may provide a potential target for novel therapeutic treatment for cardiac allograft rejection.
AB - 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 (γδ) T cells appear to be the predominant source of IL-17 production. Conclusion Therefore, IL-17 neutralization may provide a potential target for novel therapeutic treatment for cardiac allograft rejection.
KW - γδ Tcell
KW - Graft coronary artery disease
KW - IL-17
UR - http://www.scopus.com/inward/record.url?scp=77953536679&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77953536679&partnerID=8YFLogxK
U2 - 10.1007/s10875-009-9366-9
DO - 10.1007/s10875-009-9366-9
M3 - Article
C2 - 20130970
AN - SCOPUS:77953536679
SN - 0271-9142
VL - 30
SP - 235
EP - 240
JO - Journal of Clinical Immunology
JF - Journal of Clinical Immunology
IS - 2
ER -