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首页> 外文期刊>Transplantation: Official Journal of the Transplantation Society >Cardiac allograft rejection in the absence of macrophage migration inhibitory factor.
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Cardiac allograft rejection in the absence of macrophage migration inhibitory factor.

机译:在没有巨噬细胞迁移抑制因子的情况下,心脏移植排斥反应。

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BACKGROUND: Macrophage migration inhibitory factor (MIF) is a secreted proinflammatory lymphokine essential for elicitation of delayed-type hypersensitivity (DTH) reactions in vivo. We tested whether MIF blockade-absence affected acute or chronic murine cardiac allograft rejection. METHODS: Wild-type (WT) C57BL/6 (B6) mice underwent transplantation with BALB/c hearts with or without blocking anti-MIF antibody, and MIF knockout (KO) B6 mice underwent transplantation with MIF KO BALB/c hearts. Chronic immune injury was induced in WT and KO recipients using donor-specific transfusion and anti-CD40L antibody. RESULTS: Unexpectedly, the blockade or genetic absence of MIF did not prolong graft survival even if recipient T-cell cytotoxicity was additionally impaired. The histologic manifestations of acute and chronic immune injury to the allograft were similar between groups. CONCLUSIONS: MIF is not required for acute or chronic allograft rejection in mice. The findings raise questions about the role of DTH as an important mediator of cardiac allograft injury.
机译:背景:巨噬细胞迁移抑制因子(MIF)是一种分泌的促炎性淋巴因子,在体内引起迟发型超敏反应(DTH)反应至关重要。我们测试了MIF的缺失是否影响了急性或慢性鼠心脏同种异体移植排斥反应。方法:野生型(WT)C57BL / 6(B6)小鼠接受带有或不阻断抗MIF抗体的BALB / c心脏移植,MIF基因敲除(KO)B6小鼠接受MIF KO BALB / c心脏移植。使用供体特异性输血和抗CD40L抗体在WT和KO受体中诱导了慢性免疫损伤。结果:出乎意料的是,即使另外损害了受体T细胞的细胞毒性,MIF的阻断或遗传缺失也不能延长移植物的存活。两组间同种异体移植的急性和慢性免疫损伤的组织学表现相似。结论:对于小鼠的急性或慢性同种异体排斥反应,不需要MIF。这些发现提出了关于DTH作为心脏同种异体移植损伤的重要介质的作用的疑问。

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