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胰岛素依赖型糖尿病中的胰岛细胞抗原:重访潘多拉魔盒。

Islet cell antigens in insulin-dependent diabetes: Pandora's box revisited.

作者信息

Harrison L C

机构信息

Burnet Clinical Research Unit, Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Victoria, Australia.

出版信息

Immunol Today. 1992 Sep;13(9):348-52. doi: 10.1016/0167-5699(92)90170-C.

DOI:10.1016/0167-5699(92)90170-C
PMID:1466752
Abstract

A major goal of research into IDDM has been the identification of the 'causative antigen'. As described in this article by Len Harrison, this reductionist aim is confounded by the fact that numerous candidate islet cell antigens have been described. He scrutinizes the credentials of these candidates and discusses the problem of using autoantibodies to identify causative antigens in a T-cell-mediated disease.

摘要

对胰岛素依赖型糖尿病(IDDM)研究的一个主要目标是识别“致病抗原”。正如伦·哈里森在本文中所描述的,这种还原论的目标因已描述了众多候选胰岛细胞抗原这一事实而变得复杂。他仔细审查了这些候选抗原的资质,并讨论了在T细胞介导的疾病中使用自身抗体来识别致病抗原的问题。

相似文献

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Islet cell antigens in insulin-dependent diabetes: Pandora's box revisited.胰岛素依赖型糖尿病中的胰岛细胞抗原:重访潘多拉魔盒。
Immunol Today. 1992 Sep;13(9):348-52. doi: 10.1016/0167-5699(92)90170-C.
2
High T cell responses to the glutamic acid decarboxylase (GAD) isoform 67 reflect a hyperimmune state that precedes the onset of insulin-dependent diabetes.对谷氨酸脱羧酶(GAD)67亚型的高T细胞反应反映了在胰岛素依赖型糖尿病发病之前的一种超免疫状态。
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Evaluation of islet-specific autoantibodies in Japanese patients with insulin-dependent diabetes mellitus: a comparison between autoantibodies to glutamic acid decarboxylase, autoantibodies to 64 kDa islet cell protein and islet cell antibodies.日本胰岛素依赖型糖尿病患者胰岛特异性自身抗体的评估:谷氨酸脱羧酶自身抗体、64kDa胰岛细胞蛋白自身抗体与胰岛细胞抗体之间的比较
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Relation between cellular and humoral immunity to islet cell antigens in type 1 diabetes.1型糖尿病中针对胰岛细胞抗原的细胞免疫与体液免疫之间的关系。
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Contribution of glutamate decarboxylase antibodies to the reactivity of islet cell cytoplasmic antibodies.谷氨酸脱羧酶抗体对胰岛细胞胞浆抗体反应性的作用。
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[Autoantibodies in type 1 diabetes mellitus].[1型糖尿病中的自身抗体]
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Characterization of distinct islet protein autoantigens associated with type 1 diabetes.与1型糖尿病相关的不同胰岛蛋白自身抗原的特征分析。
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引用本文的文献

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Antigen targets of type 1 diabetes autoimmunity.1 型糖尿病自身免疫的抗原靶点。
Cold Spring Harb Perspect Med. 2012 Apr;2(4):a007781. doi: 10.1101/cshperspect.a007781.
2
Oral tolerance and the treatment of rheumatoid arthritis.口服耐受与类风湿关节炎的治疗
Springer Semin Immunopathol. 1998;20(1-2):289-308. doi: 10.1007/BF00832013.
3
Widespread expression of an autoantigen-GAD65 transgene does not tolerize non-obese diabetic mice and can exacerbate disease.自身抗原谷氨酸脱羧酶65(GAD65)转基因的广泛表达不能使非肥胖型糖尿病小鼠产生免疫耐受,反而会加剧疾病。
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10055-60. doi: 10.1073/pnas.95.17.10055.
4
Aerosol insulin induces regulatory CD8 gamma delta T cells that prevent murine insulin-dependent diabetes.雾化胰岛素可诱导调节性CD8γδ T细胞,预防小鼠胰岛素依赖型糖尿病。
J Exp Med. 1996 Dec 1;184(6):2167-74. doi: 10.1084/jem.184.6.2167.
5
Antigen-specific therapy for autoimmune disease: prospects for the prevention of insulin-dependent diabetes.自身免疫性疾病的抗原特异性疗法:预防胰岛素依赖型糖尿病的前景。
Mol Med. 1995 Nov;1(7):722-7.
6
Similar peptides from two beta cell autoantigens, proinsulin and glutamic acid decarboxylase, stimulate T cells of individuals at risk for insulin-dependent diabetes.来自两种β细胞自身抗原(胰岛素原和谷氨酸脱羧酶)的相似肽段,可刺激有胰岛素依赖型糖尿病风险个体的T细胞。
Mol Med. 1995 Sep;1(6):625-33.
7
The immunologic insult in type 1 diabetes.1型糖尿病中的免疫损伤。
Springer Semin Immunopathol. 1993;14(3):253-74. doi: 10.1007/BF00195977.
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Glutamic acid decarboxylase 67-reactive T cells: a marker of insulin-dependent diabetes.谷氨酸脱羧酶67反应性T细胞:胰岛素依赖型糖尿病的一个标志物。
J Exp Med. 1993 Feb 1;177(2):535-40. doi: 10.1084/jem.177.2.535.
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An autoimmune disease with multiple molecular targets abrogated by the transgenic expression of a single autoantigen in the thymus.一种自身免疫性疾病,其多个分子靶点因胸腺中单一自身抗原的转基因表达而被消除。
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Induction of anergy or active suppression following oral tolerance is determined by antigen dosage.口服耐受后无反应性或主动抑制的诱导取决于抗原剂量。
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