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

doi:10.1007/s10875-009-9366-9

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 journal › Article › peer-review

50 Scopus citations

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.

Original language	English (US)
Pages (from-to)	235-240
Number of pages	6
Journal	Journal of Clinical Immunology
Volume	30
Issue number	2
DOIs	https://doi.org/10.1007/s10875-009-9366-9
State	Published - Mar 2010
Externally published	Yes

Keywords

γδ Tcell
Graft coronary artery disease
IL-17

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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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. / Itoh, Satoshi; Nakae, Susumu; Axtell, Robert C.; Velotta, Jeffrey B.; Kimura, Naoyuki; Kajiwara, Naoki; Iwakura, Yoichiro; Saito, Hirohisa; Adachi, Hideo; Steinman, Lawrence; Robbins, Robert C.; Fischbein, Michael P.

In: Journal of Clinical Immunology, Vol. 30, No. 2, 03.2010, p. 235-240.

Research output: Contribution to journal › Article › peer-review

Itoh, Satoshi ; Nakae, Susumu ; Axtell, Robert C. ; Velotta, Jeffrey B. ; Kimura, Naoyuki ; Kajiwara, Naoki ; Iwakura, Yoichiro ; Saito, Hirohisa ; Adachi, Hideo ; Steinman, Lawrence ; Robbins, Robert C. ; Fischbein, Michael P. / IL-17 contributes to the development of chronic rejection in a murine heart transplant model. In: Journal of Clinical Immunology. 2010 ; Vol. 30, No. 2. pp. 235-240.

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

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 = "γδ Tcell, Graft coronary artery disease, IL-17",

author = "Satoshi Itoh and Susumu Nakae and Axtell, {Robert C.} and Velotta, {Jeffrey B.} and Naoyuki Kimura and Naoki Kajiwara and Yoichiro Iwakura and Hirohisa Saito and Hideo Adachi and Lawrence Steinman and Robbins, {Robert C.} and Fischbein, {Michael P.}",

note = "Funding Information: Acknowledgments This work was supported by funds from the Falk Research Fund, Department of Cardiothoracic Surgery at Stanford University Medical School, American Association for Thoracic Surgery (Norman E. Shumway award to MPF), National Institute of Biomedical Innovation (ID 05-24; H.S.), Ministry of Education, Culture, Sports, Science, and Technology (MEXT) (20790700: N.K.), and Program for Improvement of Research Environment for Young Researchers, The Special Coordination Funds for Promoting Science and Technology of MEXT (S.N.). The authors have no conflicting financial interests.",

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doi = "10.1007/s10875-009-9366-9",

language = "English (US)",

volume = "30",

pages = "235--240",

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T1 - IL-17 contributes to the development of chronic rejection in a murine heart transplant model

AU - Itoh, Satoshi

AU - Nakae, Susumu

AU - Axtell, Robert C.

AU - Velotta, Jeffrey B.

AU - Kimura, Naoyuki

AU - Kajiwara, Naoki

AU - Iwakura, Yoichiro

AU - Saito, Hirohisa

AU - Adachi, Hideo

AU - Steinman, Lawrence

AU - Robbins, Robert C.

AU - Fischbein, Michael P.

N1 - Funding Information: Acknowledgments This work was supported by funds from the Falk Research Fund, Department of Cardiothoracic Surgery at Stanford University Medical School, American Association for Thoracic Surgery (Norman E. Shumway award to MPF), National Institute of Biomedical Innovation (ID 05-24; H.S.), Ministry of Education, Culture, Sports, Science, and Technology (MEXT) (20790700: N.K.), and Program for Improvement of Research Environment for Young Researchers, The Special Coordination Funds for Promoting Science and Technology of MEXT (S.N.). The authors have no conflicting financial interests.

PY - 2010/3

Y1 - 2010/3

N2 - 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.

AB - 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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KW - Graft coronary artery disease

KW - IL-17

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

Abstract

Keywords

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