IL-17 Contributes to the Development of Chronic Rejection in a Murine Heart Transplant Model JOURNAL OF CLINICAL IMMUNOLOGY Itoh, S., Nakae, S., Axtell, R. C., Velotta, J. B., Kimura, N., Kajiwara, N., Iwakura, Y., Saito, H., Adachi, H., Steinman, L., Robbins, R. C., Fischbein, M. P. 2010; 30 (2): 235-240


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 (gammadelta) 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.

View details for DOI 10.1007/s10875-009-9366-9

View details for Web of Science ID 000275798900007

View details for PubMedID 20130970