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Arthritis Res. 2000;2(3):205-7. doi: 10.1186/ar88. Epub 2000 Apr 12.
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本文引用的文献

1
Complementation between HLA-DR4 (DRB1*0401) and specific H2-A molecule in transgenic mice leads to collagen-induced arthritis.转基因小鼠中HLA - DR4（DRB1*0401）与特定H2 - A分子之间的互补作用会导致胶原诱导的关节炎。
Hum Immunol. 1999 Sep;60(9):816-25. doi: 10.1016/s0198-8859(99)00070-1.
2
HLA class II transgenic mice as models of human diseases.HLA II类转基因小鼠作为人类疾病模型。
Immunol Rev. 1999 Jun;169:67-79. doi: 10.1111/j.1600-065x.1999.tb01307.x.
3
Identification of T cell determinants on human type II collagen recognized by HLA-DQ8 and HLA-DQ6 transgenic mice.HLA-DQ8和HLA-DQ6转基因小鼠识别的人类II型胶原蛋白上T细胞决定簇的鉴定。
J Immunol. 1999 Aug 1;163(3):1661-5.
4
Modulation of HLA-DQ-restricted collagen-induced arthritis by HLA-DRB1 polymorphism.HLA-DRB1基因多态性对HLA-DQ限制的胶原诱导性关节炎的调节作用
Int Immunol. 1998 Oct;10(10):1449-57. doi: 10.1093/intimm/10.10.1449.
5
Structural differences between HLA-DQ molecules associated with myasthenia gravis characterized by molecular modeling.通过分子建模表征的与重症肌无力相关的HLA - DQ分子之间的结构差异。
J Neuroimmunol. 1998 May 1;85(1):102-5. doi: 10.1016/s0165-5728(97)00266-x.
6
The structural basis of MHC control of collagen-induced arthritis; binding of the immunodominant type II collagen 256-270 glycopeptide to H-2Aq and H-2Ap molecules.MHC对胶原诱导性关节炎控制的结构基础；免疫显性II型胶原256 - 270糖肽与H - 2Aq和H - 2Ap分子的结合
Eur J Immunol. 1998 Feb;28(2):755-67. doi: 10.1002/(SICI)1521-4141(199802)28:02<755::AID-IMMU755>3.0.CO;2-2.
7
Induction of autoimmune arthritis in HLA-DR4 (DRB1*0401) transgenic mice by immunization with human and bovine type II collagen.通过用人和牛II型胶原蛋白免疫在HLA - DR4（DRB1*0401）转基因小鼠中诱导自身免疫性关节炎。
J Immunol. 1998 Mar 15;160(6):2573-8.
8
Critical residues on HLA-DRB1*0402 HV3 peptide for HLA-DQ8-restricted immunogenicity: implications for rheumatoid arthritis predisposition.HLA-DRB1*0402高变区3肽上对HLA-DQ8限制的免疫原性起关键作用的残基：对类风湿性关节炎易感性的影响
J Immunol. 1997 Apr 1;158(7):3545-51.
9
HLA-DQ-binding peptide motifs. 1. Comparative binding analysis of type II collagen-derived peptides to DR and DQ molecules of rheumatoid arthritis-susceptible and non-susceptible haplotypes.HLA-DQ结合肽基序。1. 类风湿关节炎易感和非易感单倍型的II型胶原衍生肽与DR和DQ分子的比较结合分析。
Int Immunol. 1996 May;8(5):757-64. doi: 10.1093/intimm/8.5.757.
10
HLA-DQ8 transgenic mice are highly susceptible to collagen-induced arthritis: a novel model for human polyarthritis.HLA-DQ8转基因小鼠对胶原诱导的关节炎高度易感：一种人类多关节炎的新型模型。
J Exp Med. 1996 Jan 1;183(1):27-37. doi: 10.1084/jem.183.1.27.

主要组织相容性复合体（MHC）与类风湿性关节炎的关联。类风湿性关节炎动物模型中HLA II类分子的调节作用：对转基因/基因敲除小鼠的研究。

Association of MHC and rheumatoid arthritis. Regulatory role of HLA class II molecules in animal models of RA: studies on transgenic/knockout mice.

作者信息

Taneja V, David C S

机构信息

Department of Immunology, Mayo Clinic, Rochester, Minnesota 55905, USA.

出版信息

Arthritis Res. 2000;2(3):205-7. doi: 10.1186/ar88. Epub 2000 Apr 12.

DOI:10.1186/ar88
PMID:11094430
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC130003/
Abstract

Human leucocyte antigen (HLA) class II molecules have been shown to be associated with predisposition to rheumatoid arthritis (RA). We generated HLA-DR and DQ transgenic mice that lacked endogenous class II molecules to study the interaction between the DR and DQ molecules and define the immunologic mechanisms in rheumatoid arthritis. Using collagen-induced arthritis (CIA) as an experimental model for inflammatory polyarthritis, we show that both DQ and DR are involved in predisposition or resistance to arthritis. Our studies suggest that polymorphism in DQB1 genes may determine predisposition to RA while the DRB1 polymorphism may dictate severity/protection of the disease. These mice provide powerful tools to develop immunotherapeutic protocols.

摘要

人类白细胞抗原（HLA）II类分子已被证明与类风湿关节炎（RA）的易感性相关。我们培育了缺乏内源性II类分子的HLA-DR和DQ转基因小鼠，以研究DR和DQ分子之间的相互作用，并确定类风湿关节炎的免疫机制。使用胶原诱导的关节炎（CIA）作为炎症性多关节炎的实验模型，我们发现DQ和DR都与关节炎的易感性或抵抗力有关。我们的研究表明，DQB1基因的多态性可能决定RA的易感性，而DRB1多态性可能决定疾病的严重程度/保护性。这些小鼠为开发免疫治疗方案提供了强大的工具。