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大鼠佐剂性关节炎

Adjuvant arthritis in the rat.

作者信息

van Eden Willem, Wagenaar-Hilbers Josee P A, Wauben Marca H M

机构信息

Institute of Infectious Diseases and Immunology, Utrecht, The Netherlands.

出版信息

Curr Protoc Immunol. 2001 May;Chapter 15:15.4.1-15.4.8. doi: 10.1002/0471142735.im1504s19.

DOI:10.1002/0471142735.im1504s19
PMID:18432736
Abstract

Adjuvant arthritis (AA) is an induced form of (sub)chronic arthritis. Strains of rats have a varying genetic susceptibility to AA, whereas mice generally are not susceptible. AA is most easily induced with mycobacteria suspended in oil, although in some strains of rats it can be induced with oily adjuvants in the absence of mycobacteria. The disease is a T cell-mediated autoimmune arthritis that is frequently used to study immunological aspects of rheumatoid arthritis (RA) and other arthritic or inflammatory diseases in humans. Furthermore, it is used as a model for developing and testing antiinflammatory drugs. There are no particularly well-defined autoantigens in AA; in this respect, the model resembles spontaneous arthritic diseases in humans. In all susceptible rat strains, the inflammatory process of AA is self remitting, although usually the disease is severe and leads to permanent joint malformations, including ankylosis; a time line for AA development is presented. This unit describes the induction and evaluation of AA and the preparation of adjuvant used to induce AA.

摘要

佐剂性关节炎(AA)是一种诱发型(亚)慢性关节炎。不同品系的大鼠对AA的遗传易感性各不相同,而小鼠通常不易感。用悬浮于油中的分枝杆菌最易诱发AA,不过在某些大鼠品系中,无分枝杆菌时用油性佐剂也可诱发。该疾病是一种T细胞介导的自身免疫性关节炎,常用于研究人类类风湿关节炎(RA)及其他关节炎或炎症性疾病的免疫学方面。此外,它还被用作开发和测试抗炎药物的模型。AA中没有特别明确的自身抗原;在这方面,该模型类似于人类的自发性关节炎疾病。在所有易感大鼠品系中,AA的炎症过程会自行缓解,尽管通常疾病较为严重并会导致永久性关节畸形,包括关节强直;文中给出了AA发展的时间线。本单元描述了AA的诱导和评估以及用于诱导AA的佐剂的制备。

相似文献

1
Adjuvant arthritis in the rat.大鼠佐剂性关节炎
Curr Protoc Immunol. 2001 May;Chapter 15:15.4.1-15.4.8. doi: 10.1002/0471142735.im1504s19.
2
The T cells specific for the carboxyl-terminal determinants of self (rat) heat-shock protein 65 escape tolerance induction and are involved in regulation of autoimmune arthritis.对自身(大鼠)热休克蛋白65羧基末端决定簇具有特异性的T细胞逃避耐受诱导,并参与自身免疫性关节炎的调节。
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Environmental modulation of autoimmune arthritis involves the spontaneous microbial induction of T cell responses to regulatory determinants within heat shock protein 65.自身免疫性关节炎的环境调节涉及微生物对热休克蛋白65内调节决定簇的T细胞反应的自发诱导。
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Relationship between collagen-induced and adjuvant arthritis in the Lewis rat.胶原诱导性关节炎与佐剂性关节炎在Lewis大鼠中的关系。
J Autoimmun. 1993 Dec;6(6):691-700. doi: 10.1006/jaut.1993.1058.
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The determinants of susceptibility/resistance to adjuvant arthritis in rats.大鼠对佐剂性关节炎易感性/抗性的决定因素。
Arthritis Res Ther. 2009;11(4):239. doi: 10.1186/ar2755. Epub 2009 Aug 7.
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Strain differences and the role for HSP47 and HSP70 in adjuvant arthritis in rats.
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Triptolide inhibits CC chemokines expressed in rat adjuvant-induced arthritis.雷公藤甲素抑制大鼠佐剂性关节炎中表达的CC趋化因子。
Int Immunopharmacol. 2006 Dec 5;6(12):1825-32. doi: 10.1016/j.intimp.2006.07.029. Epub 2006 Aug 31.
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Antibody responses to mycobacterial and self heat shock protein 65 in autoimmune arthritis: epitope specificity and implication in pathogenesis.自身免疫性关节炎中针对分枝杆菌和自身热休克蛋白65的抗体反应:表位特异性及其在发病机制中的意义。
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Regulation of autoimmune arthritis by the pro-inflammatory cytokine interferon-gamma.促炎细胞因子γ干扰素对自身免疫性关节炎的调控
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10
T cell reactivity to an epitope of the mycobacterial 65-kDa heat-shock protein (hsp 65) corresponds with arthritis susceptibility in rats and is regulated by hsp 65-specific cellular responses.T细胞对分枝杆菌65-kDa热休克蛋白(hsp 65)表位的反应性与大鼠关节炎易感性相关,并受hsp 65特异性细胞反应调控。
Eur J Immunol. 1991 May;21(5):1289-96. doi: 10.1002/eji.1830210529.

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