IL-17 contributes to the development of chronic rejection in a murine heart transplant model

Satoshi Itoh, 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

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)235-240
Number of pages6
JournalJournal of Clinical Immunology
Issue number2
StatePublished - Mar 2010
Externally publishedYes


  • γδ Tcell
  • Graft coronary artery disease
  • IL-17

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


Dive into the research topics of 'IL-17 contributes to the development of chronic rejection in a murine heart transplant model'. Together they form a unique fingerprint.

Cite this