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HLA - B27转基因动物中的关节炎。

Arthritis in HLA-B27 transgenic animals.

作者信息

Taurog J D

机构信息

Harold C. Simmons Arthritis Research Center, University of Texas Southwestern Medical Center, Dallas 75235-8884, USA.

出版信息

Am J Med Sci. 1998 Oct;316(4):250-6. doi: 10.1097/00000441-199810000-00005.

DOI:10.1097/00000441-199810000-00005
PMID:9766486
Abstract

This review focuses on investigations of rats and mice transgenic for HLA-B27; these animals have been investigated for several years as potential models for the human spondyloarthropathies. Spontaneous multisystem disease occurs in rats with high expression of B27 and human beta2-microglobulin (hbeta2m). The disease is T-cell-dependent and is sensitive to both environmental and genetic manipulation. A spontaneous arthritis and enthesopathy has been observed by some investigators in nontransgenic mice which seems to be more prevalent in B27 transgenic mice. Peripheral arthritis has also been reported in B27 transgenic mice that lack mouse beta2m. Potential insights from these animals into the pathogenesis of B27-related disease are discussed.

摘要

本综述聚焦于HLA - B27转基因大鼠和小鼠的研究;这些动物作为人类脊柱关节病的潜在模型已被研究数年。B27和人β2微球蛋白(hβ2m)高表达的大鼠会发生自发性多系统疾病。该疾病依赖于T细胞,对环境和基因操作均敏感。一些研究者在非转基因小鼠中观察到了自发性关节炎和附着点病,这在B27转基因小鼠中似乎更为普遍。在缺乏小鼠β2m的B27转基因小鼠中也报道了外周关节炎。本文讨论了这些动物对B27相关疾病发病机制的潜在见解。

相似文献

1
Arthritis in HLA-B27 transgenic animals.HLA - B27转基因动物中的关节炎。
Am J Med Sci. 1998 Oct;316(4):250-6. doi: 10.1097/00000441-199810000-00005.
2
Spontaneous inflammatory arthritis in HLA-B27 transgenic mice lacking beta 2-microglobulin: a model of human spondyloarthropathies.缺乏β2-微球蛋白的HLA-B27转基因小鼠的自发性炎性关节炎:一种人类脊柱关节病模型
J Exp Med. 1995 Oct 1;182(4):1153-8. doi: 10.1084/jem.182.4.1153.
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Additional human beta2-microglobulin curbs HLA-B27 misfolding and promotes arthritis and spondylitis without colitis in male HLA-B27-transgenic rats.额外的人β2-微球蛋白可抑制男性HLA-B27转基因大鼠中HLA-B27的错误折叠,并促进关节炎和脊柱炎的发生,而不会引发结肠炎。
Arthritis Rheum. 2006 Apr;54(4):1317-27. doi: 10.1002/art.21740.
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HLA-B27 transgenic rats: animal model of human HLA-B27-associated disorders.
Toxicol Pathol. 1997 Jul-Aug;25(4):407-8. doi: 10.1177/019262339702500411.
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HLA-B27 heavy chain homodimers are expressed in HLA-B27 transgenic rodent models of spondyloarthritis and are ligands for paired Ig-like receptors.HLA - B27重链同型二聚体在脊柱关节炎的HLA - B27转基因啮齿动物模型中表达,并且是配对免疫球蛋白样受体的配体。
J Immunol. 2004 Aug 1;173(3):1699-710. doi: 10.4049/jimmunol.173.3.1699.
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[New aspects in the pathogenesis of Bechterew disease].[贝赫切特病发病机制的新进展]
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HLA-B27 heavy chains contribute to spontaneous inflammatory disease in B27/human beta2-microglobulin (beta2m) double transgenic mice with disrupted mouse beta2m.HLA - B27重链在小鼠β2微球蛋白(β2m)基因敲除的B27/人β2微球蛋白(β2m)双转基因小鼠中引发自发性炎症疾病。
J Clin Invest. 1996 Dec 15;98(12):2746-55. doi: 10.1172/JCI119100.
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HLA-B27 transgenic rats model.HLA - B27转基因大鼠模型。
Ann Med Interne (Paris). 1998 Apr;149(3):139-41.
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The mystery of HLA-B27 and disease.人类白细胞抗原B27与疾病之谜。
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Inducible nitric oxide synthase attenuates chronic colitis in human histocompatibility antigen HLA-B27/human beta2 microglobulin transgenic rats.诱导型一氧化氮合酶减轻人类组织相容性抗原HLA - B27/人类β2微球蛋白转基因大鼠的慢性结肠炎。
Eur Cytokine Netw. 2001 Mar;12(1):111-8.

引用本文的文献

1
The utility of pathway selective estrogen receptor ligands that inhibit nuclear factor-kappa B transcriptional activity in models of rheumatoid arthritis.在类风湿性关节炎模型中抑制核因子-κB转录活性的通路选择性雌激素受体配体的效用。
Arthritis Res Ther. 2005;7(3):R427-38. doi: 10.1186/ar1692. Epub 2005 Feb 21.
2
HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations.HLA - B27相关反应性关节炎:发病机制与临床考量
Clin Microbiol Rev. 2004 Apr;17(2):348-69. doi: 10.1128/CMR.17.2.348-369.2004.
3
Animal models of ankylosing spondylitis.
强直性脊柱炎的动物模型。
Curr Rheumatol Rep. 2002 Dec;4(6):507-12. doi: 10.1007/s11926-002-0058-1.
4
A molecular insight on the association of HLA-B27 with spondyloarthropathies.关于HLA - B27与脊柱关节病关联的分子见解。
Curr Rheumatol Rep. 1999 Oct;1(1):78-85. doi: 10.1007/s11926-999-0029-x.