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白细胞介素6型细胞因子的血液病理学

Hematopathology of interleukin 6-type cytokines.

作者信息

Hawley R G

机构信息

Division of Cancer Research, Sunnybrook Health Science Centre, Toronto, Ontario, Canada.

出版信息

Stem Cells. 1994;12 Suppl 1:155-71.

PMID:7696960
Abstract

Interleukin (IL)-6, IL-11, leukemia inhibitory factor (LIF), oncostatin M (OSM) and ciliary neurotrophic factor (CNTF) constitute a subfamily of cytokines on the basis of similar predicted structures and functional redundancy in their actions on a wide spectrum of cell types. Among the diverse targets of these pleiotropic factors are adipocytes, embryonic stem cells, hepatocytes, and cells belonging to the hematopoietic, immune and nervous systems. An explanation for the shared biologic activities of IL-6 subfamily members is provided by the finding that these cytokines trigger overlapping signal transduction pathways in responsive cells through a common receptor subunit, termed gp130. With the exception of CNTF, which appears to function primarily within the nervous system, IL-6-type cytokines differ from classical hormones in that they are synthesized by many tissues, frequently in association with disease states or in response to infection or injury. This article discusses the hematologic effects of dysregulated expression of IL-6 and related cytokines, highlighting results obtained in our laboratory with murine models of cytokine excess created by retroviral gene delivery to the hematopoietic system.

摘要

白细胞介素(IL)-6、IL-11、白血病抑制因子(LIF)、抑瘤素M(OSM)和睫状神经营养因子(CNTF)基于其相似的预测结构以及对多种细胞类型作用的功能冗余性,构成了一个细胞因子亚家族。这些多效性因子的不同靶细胞包括脂肪细胞、胚胎干细胞、肝细胞以及造血、免疫和神经系统的细胞。这些白细胞介素-6亚家族成员具有共同生物学活性的一个解释是,发现这些细胞因子通过一个称为gp130的共同受体亚基,在反应性细胞中触发重叠的信号转导途径。除了主要在神经系统内发挥作用的CNTF外,白细胞介素-6型细胞因子与经典激素不同,因为它们由许多组织合成,常常与疾病状态相关,或对感染或损伤作出反应。本文讨论白细胞介素-6及相关细胞因子表达失调的血液学效应,重点介绍我们实验室利用逆转录病毒基因导入造血系统建立的细胞因子过量小鼠模型所获得的结果。

相似文献

1
Hematopathology of interleukin 6-type cytokines.白细胞介素6型细胞因子的血液病理学
Stem Cells. 1994;12 Suppl 1:155-71.
2
Signal transduction through gp130 that is shared among the receptors for the interleukin 6 related cytokine subfamily.通过gp130的信号转导,这在白细胞介素6相关细胞因子亚家族的受体中是共享的。
Stem Cells. 1994 May;12(3):262-77. doi: 10.1002/stem.5530120303.
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The cytokine receptor gp130: faithfully promiscuous.细胞因子受体gp130:忠实的混杂性
Sci STKE. 2003 Sep 23;2003(201):PE40. doi: 10.1126/stke.2003.201.pe40.
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gp130 and the IL-6 family of cytokines: signaling mechanisms and thrombopoietic activities.gp130与白细胞介素-6细胞因子家族:信号传导机制及血小板生成活性
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FR901228, an inhibitor of histone deacetylases, increases the cellular responsiveness to IL-6 type cytokines by enhancing the expression of receptor proteins.FR901228,一种组蛋白脱乙酰酶抑制剂,通过增强受体蛋白的表达来提高细胞对IL-6型细胞因子的反应性。
Oncogene. 2002 Sep 12;21(41):6264-77. doi: 10.1038/sj.onc.1205777.
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Characterization of soluble gp130 released by melanoma cell lines: A polyvalent antagonist of cytokines from the interleukin 6 family.黑色素瘤细胞系释放的可溶性gp130的特性:一种白细胞介素6家族细胞因子的多价拮抗剂。
Clin Cancer Res. 1997 Aug;3(8):1443-51.
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Interleukin 11: an overview.白细胞介素11:概述
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The human IL-11 receptor requires gp130 for signalling: demonstration by molecular cloning of the receptor.人白细胞介素-11受体信号传导需要gp130:通过受体的分子克隆证明
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Activation of the signal transducer glycoprotein 130 by both IL-6 and IL-11 requires two distinct binding epitopes.白细胞介素-6和白细胞介素-11对信号转导蛋白糖蛋白130的激活需要两个不同的结合表位。
J Immunol. 1999 Feb 1;162(3):1480-7.
10
Interleukin-11 and its receptor.白细胞介素-11及其受体。
Biofactors. 1992 Dec;4(1):15-21.

引用本文的文献

1
Serum levels of IL-6 type cytokines and soluble IL-6 receptors in active B-cell chronic lymphocytic leukemia and in cladribine induced remission.活动性B细胞慢性淋巴细胞白血病及克拉屈滨诱导缓解期的血清IL-6型细胞因子和可溶性IL-6受体水平
Mediators Inflamm. 1999;8(6):277-86. doi: 10.1080/09629359990289.
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Serum levels of interleukin-6 type cytokines and soluble interleukin-6 receptor in patients with rheumatoid arthritis.类风湿关节炎患者血清白细胞介素-6 型细胞因子及可溶性白细胞介素-6 受体水平
Mediators Inflamm. 1998;7(5):347-53. doi: 10.1080/09629359890875.
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Thrombopoietic potential and serial repopulating ability of murine hematopoietic stem cells constitutively expressing interleukin 11.
Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10297-302. doi: 10.1073/pnas.93.19.10297.