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Genes for MHC, TCR and MIs determine susceptibility to collagen induced arthritis.

作者信息

David C S

机构信息

Department of Immunology, Mayo Clinic, Rochester, MN 55905.

出版信息

APMIS. 1990 Jul;98(7):575-84. doi: 10.1111/j.1699-0463.1990.tb04974.x.

DOI:10.1111/j.1699-0463.1990.tb04974.x
PMID:1697756
Abstract

Type II collagen induced arthritis (CIA) in mice is an animal model for polyarthritis. The susceptibility to the disease is linked to the class II genes of H-2 gene complex (MHC). The susceptibility requires T cells expressing certain receptors coded by the V beta genes. Further, the MIs gene products in combination with the class II molecules can up- or down-regulate the T cells involved in the disease. The disease is mediated by the presentation of an arthritogenic epitope on the collagen type II peptide by the MHC class II molecule, which is recognized by a T cell expressing certain V beta receptors, triggering the autoimmune response. These studies point out possible mechanisms of rheumatoid arthritis in humans and suggest various methods of immune intervention to down-regulate the disease.

摘要

相似文献

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引用本文的文献

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2
IFNgamma deficient C57BL/6 (H-2b) mice develop collagen induced arthritis with predominant usage of T cell receptor Vbeta6 and Vbeta8 in arthritic joints.干扰素γ缺陷的C57BL/6(H-2b)小鼠会发生胶原诱导性关节炎,关节炎关节中T细胞受体Vβ6和Vβ8的使用占主导。
Ann Rheum Dis. 2003 Oct;62(10):983-90. doi: 10.1136/ard.62.10.983.
3
Amelioration of collagen-induced arthritis by CD95 (Apo-1/Fas)-ligand gene transfer.
通过CD95(Apo-1/Fas)配体基因转移改善胶原诱导的关节炎。
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Immune response of HLA-DQ8 transgenic mice to peptides from the third hypervariable region of HLA-DRB1 correlates with predisposition to rheumatoid arthritis.HLA-DQ8转基因小鼠对HLA-DRB1第三个高变区肽段的免疫反应与类风湿关节炎易感性相关。
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