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
Journal of Clinical Immunology
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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 (γδ) 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.