Humanized mice as a model for rheumatoid arthritis

被引：10

作者：

Eming, Ruediger ^{[1
]}

Visconti, Kevin ^{[1
]}

Hall, Frances ^{[1
,2
]}

Sekine, Chiyoko ^{[1
]}

Kobayashi, Kayta ^{[1
]}

Chen, Qun ^{[1
]}

Cope, Andrew ^{[1
,3
]}

Kanazawa, Satoshi ^{[4
]}

Peterlin, Matija ^{[4
]}

Rijnders, Antonius ^{[5
]}

Boots, Annemieke ^{[5
]}

Meijerink, Jan ^{[5
]}

Sonderstrup, Grete ^{[1
]}

机构：

[1] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Sherman Fairchild Bldg,Room D345,299 Campus Dr, Stanford, CA 94305 USA

[2] Weatherall Inst Mol Med, Oxford, England

[3] Imperial Coll, Kennedy Inst Rheumatol, London, England

[4] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA

[5] NV Organon, NL-5340 BH Oss, Netherlands

来源：

ARTHRITIS RESEARCH & THERAPY | 2002年 / 4卷 / Suppl 3期

关键词：

autoimmunity; HCgp-39; HLA-DR4 transgenic mice; rheumatoid arthritis; T-cell receptor transgenic mice;

D O I：

10.1186/ar580

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Genetic susceptibility to rheumatoid arthritis (RA), a common autoimmune disease, is associated with certain HLA-DR4 alleles. Treatments are rarely curative and are often tied to major side effects. We describe the development of a humanized mouse model wherein new, less toxic, vaccine-like treatments for RA might be pretested. This model includes four separate transgenes: HLA-DR*0401 and human CD4 molecules, a RA-related human autoantigenic protein (HCgp-39), and a T-cell receptor (TCR alpha beta) transgene specific for an important HCgp-39 epitope, eliciting strong Th1 responses in the context of HLA-DR*0401.

引用

页码：S133 / S140

页数：8

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