Interleukin-23 Promotes Natural Killer T-Cell Production of IL-17 during Rat Liver Transplantation
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作者:
Liu, X. C.
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Cent S Univ, Xiangya Hosp 2, Dept Organ Transplantat, Changsha, Hunan, Peoples R ChinaCent S Univ, Xiangya Hosp 2, Dept Organ Transplantat, Changsha, Hunan, Peoples R China
Liu, X. C.
[1
]
Zhai, A.
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Changsha Cent Hosp, Ctr Treatment Lung Dis, Changsha, Hunan, Peoples R ChinaCent S Univ, Xiangya Hosp 2, Dept Organ Transplantat, Changsha, Hunan, Peoples R China
Zhai, A.
[2
]
Li, J. Q.
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Cent S Univ, Xiangya Hosp 2, Dept Organ Transplantat, Changsha, Hunan, Peoples R ChinaCent S Univ, Xiangya Hosp 2, Dept Organ Transplantat, Changsha, Hunan, Peoples R China
Li, J. Q.
[1
]
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Qi, H. Z.
[1
]
机构:
[1] Cent S Univ, Xiangya Hosp 2, Dept Organ Transplantat, Changsha, Hunan, Peoples R China
[2] Changsha Cent Hosp, Ctr Treatment Lung Dis, Changsha, Hunan, Peoples R China
Introduction. Cytokine interleukin-17 (IL-17) is a key proinflammatory mediator promoting allograft cytokine and chemokine production. In addition to Th17 cells, natural killer T (NKT) cells have also been shown to be capable of rapidly producing IL-17 after activation. Methods. The levels of IL-17 and IL-23 of liver allografts were determined using enzyme-linked immunosorbent assay (ELISA). IL-17 positive cells in CD1d CD4+ cells of grafts were detected using flow cytometry. Results. High expression of IL-17 and IL-23 was observed in liver allografts. The ratios of NKT cells were dramatically increased in the allograft group compared with that in the control group (P < .01). In vitro, blockage of IL-23 using anti-IL-23 antibody can inhibit increasing expression of IL-17 (P < .01). Conclusion. NKT cells contribute to production of IL-17 mediated by IL-23 on a rat acute allograft rejection model of orthotopic liver transplantation (OLT).
机构:
Marques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Fabrega, Emilio
;
Lopez-Hoyos, Marcos
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Marques de Valdecilla Univ Hosp, Fac Med, Immunol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Lopez-Hoyos, Marcos
;
Segundo, David San
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Marques de Valdecilla Univ Hosp, Fac Med, Immunol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Segundo, David San
;
Casafont, Fernandoo
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Marques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Casafont, Fernandoo
;
Pons-Romero, Fernando
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Marques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
机构:
Marques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Fabrega, Emilio
;
Lopez-Hoyos, Marcos
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Marques de Valdecilla Univ Hosp, Fac Med, Immunol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Lopez-Hoyos, Marcos
;
Segundo, David San
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Marques de Valdecilla Univ Hosp, Fac Med, Immunol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Segundo, David San
;
Casafont, Fernandoo
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Marques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain
Casafont, Fernandoo
;
Pons-Romero, Fernando
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Marques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, SpainMarques de Valdecilla Univ Hosp, Fac Med, Gastroenterol & Hepatol Unit, Santander 39008, Spain