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γ干扰素在移植物抗宿主病脾脏和正常骨髓中具有自然抑制活性的证据。

Evidence that IFN-gamma is responsible for natural suppressor activity in GVHD spleen and normal bone marrow.

作者信息

Holda J H, Maier T, Claman H N

机构信息

Department of Medicine, University of Colorado School of Medicine, Denver 80262.

出版信息

Transplantation. 1988 Apr;45(4):772-7. doi: 10.1097/00007890-198804000-00021.

DOI:10.1097/00007890-198804000-00021
PMID:2965835
Abstract

Natural suppressor (NS) cells are capable of suppressing immunological responses in a nonspecific manner. Previously, we have described NS cells in the spleens of mice undergoing chronic graft-versus-host disease (GVHD) and also in normal B10.D2 bone marrow (BM). NS cells obtained from these environments appear dependent upon lymphokines for their ability to manifest suppression. In this report, with anti-IFN-gamma antibody, we show that IFN-gamma is necessary for NS cell activation. Anti-IFN-gamma antibody is able to remove the ability of NS cells to suppress a concanavalin A (Con A) proliferation assay. Also, anti-IFN-gamma antibody removes the ability of rIL-2, lectin-free Con A supernate (CAS), and recombinant IFN-gamma (rIFN-gamma) to enhance NS suppression of lipopolysaccharide response. By these criteria, IFN-gamma is required for NS cell activation, and rIL-2 may act indirectly by its ability to stimulate IFN-gamma synthesis. These results are discussed in the context of the immuno-suppression seen in human BM transplantation.

摘要

天然抑制细胞(NS细胞)能够以非特异性方式抑制免疫反应。此前,我们曾描述过慢性移植物抗宿主病(GVHD)小鼠脾脏以及正常B10.D2骨髓(BM)中的NS细胞。从这些环境中获得的NS细胞表现出的抑制能力似乎依赖于淋巴因子。在本报告中,我们使用抗γ干扰素抗体表明,γ干扰素是NS细胞激活所必需的。抗γ干扰素抗体能够消除NS细胞抑制刀豆蛋白A(Con A)增殖试验的能力。此外,抗γ干扰素抗体还能消除重组白细胞介素-2(rIL-2)、无凝集素Con A上清液(CAS)和重组γ干扰素(rIFN-γ)增强NS细胞对脂多糖反应抑制的能力。根据这些标准,γ干扰素是NS细胞激活所必需的,而rIL-2可能通过刺激γ干扰素合成的能力间接发挥作用。我们将在人类骨髓移植中所见免疫抑制的背景下讨论这些结果。

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Evidence that IFN-gamma is responsible for natural suppressor activity in GVHD spleen and normal bone marrow.γ干扰素在移植物抗宿主病脾脏和正常骨髓中具有自然抑制活性的证据。
Transplantation. 1988 Apr;45(4):772-7. doi: 10.1097/00007890-198804000-00021.
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引用本文的文献

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A defect in interleukin 12-induced activation and interferon gamma secretion of peripheral natural killer T cells in nonobese diabetic mice suggests new pathogenic mechanisms for insulin-dependent diabetes mellitus.非肥胖糖尿病小鼠外周自然杀伤T细胞中白细胞介素12诱导的激活及γ干扰素分泌缺陷提示胰岛素依赖型糖尿病新的致病机制。
J Exp Med. 1999 Oct 4;190(7):963-72. doi: 10.1084/jem.190.7.963.
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Donor-derived interferon gamma is required for inhibition of acute graft-versus-host disease by interleukin 12.供体来源的干扰素γ是白细胞介素12抑制急性移植物抗宿主病所必需的。
J Clin Invest. 1998 Dec 15;102(12):2126-35. doi: 10.1172/JCI4992.
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Alterations in frequency of interleukin-2 (IL-2)-, gamma interferon-, or IL-4-secreting splenocytes induced by Candida albicans mannan and/or monophosphoryl lipid A.
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Infect Immun. 1998 Apr;66(4):1392-9. doi: 10.1128/IAI.66.4.1392-1399.1998.
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Clin Diagn Lab Immunol. 1997 Nov;4(6):764-8. doi: 10.1128/cdli.4.6.764-768.1997.
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