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01.03.2010

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

verfasst von: 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

Erschienen in: Journal of Clinical Immunology | Ausgabe 2/2010

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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.

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Titel: IL-17 Contributes to the Development of Chronic Rejection in a Murine Heart Transplant Model
verfasst von: 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
Publikationsdatum: 01.03.2010
Verlag: Springer US
Erschienen in: Journal of Clinical Immunology / Ausgabe 2/2010
Print ISSN: 0271-9142
Elektronische ISSN: 1573-2592
DOI: https://doi.org/10.1007/s10875-009-9366-9

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

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