Journal of Clinical Immunology

, Volume 30, Issue 2, pp 235–240

IL-17 Contributes to the Development of Chronic Rejection in a Murine Heart Transplant Model

Authors

  • Satoshi Itoh
    • Department of Cardiothoracic SurgeryStanford University School of Medicine
    • Department of Cardiovascular Surgery, Saitama Medical CenterJichi Medical University
  • Susumu Nakae
    • Department of Allergy and ImmunologyNational Research Institute for Child Health and Development
    • Atopy Research CenterJuntendo University
    • Frontier Research Initiative, The Institute of Medical ScienceUniversity of Tokyo
  • Robert C. Axtell
    • Department of Neurology and Neurological SciencesStanford University School of Medicine
  • Jeffrey B. Velotta
    • Department of Cardiothoracic SurgeryStanford University School of Medicine
  • Naoyuki Kimura
    • Department of Cardiothoracic SurgeryStanford University School of Medicine
  • Naoki Kajiwara
    • Department of Allergy and ImmunologyNational Research Institute for Child Health and Development
    • Atopy Research CenterJuntendo University
  • Yoichiro Iwakura
    • Center for Experimental Medicine, The Institute of Medical ScienceUniversity of Tokyo
  • Hirohisa Saito
    • Department of Allergy and ImmunologyNational Research Institute for Child Health and Development
    • Atopy Research CenterJuntendo University
  • Hideo Adachi
    • Department of Cardiovascular Surgery, Saitama Medical CenterJichi Medical University
  • Lawrence Steinman
    • Department of Neurology and Neurological SciencesStanford University School of Medicine
  • Robert C. Robbins
    • Department of Cardiothoracic SurgeryStanford University School of Medicine
    • Department of Cardiothoracic SurgeryStanford University School of Medicine
Article

DOI: 10.1007/s10875-009-9366-9

Cite this article as:
Itoh, S., Nakae, S., Axtell, R.C. et al. J Clin Immunol (2010) 30: 235. doi:10.1007/s10875-009-9366-9

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 (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.

Keywords

IL-17graft coronary artery diseaseγδ T cell

Copyright information

© Springer Science+Business Media, LLC 2010