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English Journal
- Anti-interleukin-12/23p40 antibody attenuates chronic rejection of cardiac allografts partly via inhibition γδT cells.
- Wang S1, Xu X, Xie A, Li J, Ye P, Liu Z, Wu J, Rui L, Xia J.Author information 1Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Institute of Cardiovascular Surgery, Xijing Hospital, The 4th Military Medical University, Xi'an, Shaanxi Province Department of Cardiovascular Surgery, Fu Wai Hospital, Beijing, China.AbstractIn our previous study, we showed that treatment with an anti-interleukin (IL)-12/23p40 antibody inhibits acute cardiac allograft rejection via inhibiting production of interferon (IFN)-γ and IL-17a. However, the impact of this antagonistic anti-p40 antibody on chronic cardiac rejection was unclear. Hearts of B6.C-H2bm12/KhEg mice were transplanted into major histocompatibility complex (MHC) class II-mismatched C57Bl/6J mice (wild-type, γδTCR (-/-) and IL-17(-/-) ), which is an established murine model of chronic allograft rejection without immunosuppression. The mice were treated with control immunoglobulin (Ig)G or 200 µg anti-p40 monoclonal antibody on post-operative days, respectively. Abdominal palpation and echocardiography were used to monitor graft survival. The mice administered with anti-p40 antibody showed a significant promotion in graft survival (median survival time >100 days), and histological analyses revealed that cardiac allograft rejection was attenuated. Quantitative real-time polymerase chain reaction (qRT-PCR) and immunofluorescence analyses demonstrated that anti-p40 antibody down-regulated the level of ingraft cytokine and chemokine expression (IL-6, IFN-γ, IL-17a, CCL2 and CCL20). Flow cytometry analyses showed that γδ T cells are an important ingraft source of IFN-γ and IL-17a and inhibit the production of inflammation cytokine by anti-p40 antibody. Compared with the wild-type group, the graft survival time in the γδ T cell receptor(-/-) and IL-17(-/-) mice was prolonged significantly. Therefore we propose that, in the chronic allograft rejection model, treatment with anti-p40 antibody prolongs graft survival possibly by reducing the amount of reactive inflammatory cells, especially γδ T cells.
- Clinical and experimental immunology.Clin Exp Immunol.2012 Sep;169(3):320-9. doi: 10.1111/j.1365-2249.2012.04612.x.
- In our previous study, we showed that treatment with an anti-interleukin (IL)-12/23p40 antibody inhibits acute cardiac allograft rejection via inhibiting production of interferon (IFN)-γ and IL-17a. However, the impact of this antagonistic anti-p40 antibody on chronic cardiac rejection was unclear.
- PMID 22861372
- Ingraft chimerism in lung transplantation--a study in a porcine model of obliterative bronchiolitis.
- Päiväniemi OE1, Musilova P, Raivio PM, Maasilta PK, Alho HS, Rubes J, Aittomäki K, Salminen US.Author information 1Department of Cardiothoracic Surgery, Helsinki University Hospital, University of Helsinki, P.O. Box 340, 00029 HUS, Helsinki, Finland. outi.paivaniemi@fimnet.fiAbstractBACKGROUND: Bronchial epithelium is a target of the alloimmune response in lung transplantation, and intact epithelium may protect allografts from rejection and obliterative bronchiolitis (OB). Herein we study the influence of chimerism on bronchial epithelium and OB development in pigs.
- Respiratory research.Respir Res.2011 Apr 26;12:56. doi: 10.1186/1465-9921-12-56.
- BACKGROUND: Bronchial epithelium is a target of the alloimmune response in lung transplantation, and intact epithelium may protect allografts from rejection and obliterative bronchiolitis (OB). Herein we study the influence of chimerism on bronchial epithelium and OB development in pigs.METHODS: A t
- PMID 21521503
- Intragraft TGF-beta 1 mRNA: a correlate of interstitial fibrosis and chronic allograft nephropathy.
- Sharma VK1, Bologa RM, Xu GP, Li B, Mouradian J, Wang J, Serur D, Rao V, Suthanthiran M.Author information 1Rogosin Institute, Department of Transplantation Medicine and Extracorporeal Therapy, New York Hospital-Cornell Medical Center, New York, USA.AbstractChronic allograft nephropathy is a relentlessly progressive process and a major cause of long-term graft dysfunction and ultimate failure. Interstitial fibrosis, tubular atrophy, and glomerular and vascular lesions characterize this mechanistically unresolved disorder. Given the prominent role of TGF-beta 1 in tissue repair and in fibrosis, we have explored the hypothesis that fibrosis and chronic allograft nephropathy would be distinguished by intragraft TGF-beta 1 mRNA expression. This postulate was tested by mRNA phenotyping of RNA isolated from 127 human renal allograft biopsies. Reverse transcription assisted polymerase chain reaction was used to amplify and identify ingraft gene expression. Our investigation demonstrated a significant correlation between intragraft TGF-beta 1 mRNA display and renal allograft interstitial fibrosis and chronic allograft nephropathy. In contrast, intragraft expression of mRNA encoding immunoregulatory cytokines, IL-2, IFN-gamma, IL-4, IL-10, or cytotoxic attack molecules, granzyme B and perforin was not a correlate of interstitial fibrosis or chronic allograft nephropathy. Our studies identify, for the first time, a significant association between intragraft TGF-beta 1 mRNA expression and renal allograft interstitial fibrosis, and advance a candidate molecular mechanism for chronic allograft nephropathy.
- Kidney international.Kidney Int.1996 May;49(5):1297-303.
- Chronic allograft nephropathy is a relentlessly progressive process and a major cause of long-term graft dysfunction and ultimate failure. Interstitial fibrosis, tubular atrophy, and glomerular and vascular lesions characterize this mechanistically unresolved disorder. Given the prominent role of TG
- PMID 8731094
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- ingraft / ɪnˈgræft, -ˈgrɑft / Show Spelled [in-graft, - grahft] Show IPA verb (used with object) engraft. Related forms ingraftment, ingraftation, noun uningrafted, adjective Dictionary.com Unabridged Based on the Random House ...
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