期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

蛋白聚糖诱导小鼠关节炎模型的研究进展 被引量：6

Proteoglycan-induced arthritis model in mice:research progress
下载PDF
导出
摘要 蛋白聚糖诱导的小鼠关节炎模型(PGIA)是由人类关节软骨来源的蛋白聚糖免疫BALB/c小鼠或C3H小鼠的某些亚系而产生的系统性自身免疫性脊柱关节炎小鼠模型。该模型是目前唯一侵犯中轴骨系统的系统性自身免疫小鼠模型,已成为脊柱关节炎动物模型的研究热点。本文旨在通过回顾国内外PGIA相关研究文献,对普遍关注的PGIA动物模型的诱导、表型鉴定、免疫学特性及骨化相关信号通路等进行综述,为脊柱关节炎动物模型研究提供理论基础。 Proteoglycan-induced arthritis （PGIA） is a unique systemic autoimmune disease model of spondyloarthritis （SPA） induced by intraperitoneal immunization of either BALB/c or certain C3H colonies with cartilage proteoglycan. This model is currently the only systemic autoimmune mice model with axial skeleton manifestation, which has become a focus of study in SpA modeling. Here in this review we summarize the methods of animal model building, phenotype identification, immunological characteristics and pathways involved in bone remodeling of PGIA based on previous studies, hoping to provide references for study on SpA animal model.
作者 童文文 李甲 徐卫东
机构地区 第二军医大学长海医院关节骨病外科
出处 《第二军医大学学报》 CAS CSCD 北大核心 2015年第5期530-535,共6页 Academic Journal of Second Military Medical University
关键词 脊柱关节炎 蛋白聚糖类 动物模型 小鼠 免疫 spondyloarthritis proteoglycans animal models mice immunity
分类号 R684.3 [医药卫生—骨科学] R-332 [医药卫生]
  • 相关文献

参考文献35

  • 1Bdrdos T, Szab6 Z, Czipri M, Vermes C, Tunyogi- Csap6 M, Urban R M, et al. A longitudinal study on an autoimmune murine model of ankylosing spondylitis [J]. Ann Rheum Dis, 2005,64.. 981-987.
  • 2Farkas B, Boldizsar F, Tarjanyi O, Laszlo A, Lin S M, Hutas G, et al. BALB/c mice genetically suscepti- ble to proteoglycan-induced arthritis and spondylitis show colony-dependent differences in disease pene- trance[J]. Arthritis Res Ther, 2009,11 : R21.
  • 3Glant T T, tMrdos T, Vermes C, Chandrasekaran R, Vald6z J C, Otto J M, et al. Variations in susceptibili- ty to proteoglycan-induced arthritis and spondylitis a- mong C3H substrains of mice: evidence of genetically acquired resistance to autoimmune disease[J]. Arthri- tis Rheum, 2001,44 : 682-692.
  • 4Adarichev V A, Valdez J C, tMrdos T, Finnegan A, Mikecz K, Glant T T. Combined autoimmune models of arthritis reveal shared and independent qualitative (binary) and quantitative trait loci[J]. J Immunol, 2003,170 .. 2283-2292.
  • 5Glant T T, Adarichev V A, Boldizsar F, Besenyei T, Laszlo A, Mikecz K, et al. Disease-promoting and - protective genomic loci on mouse chromosomes 3 and 19 control the incidence and severity of autoimmune ar- thritis[J]. Genes Immun, 2012,13.. 336-345.
  • 6Glant T T, Finnegan A, Mikecz K. Proteoglycan-in- duced arthritis: immune regulation, cellular mecha- nisms, and genetics[J]. Crit Rev Immunol, 2003,23: 199-250.
  • 7Glant T T, Mikecz K. Proteoglycan aggrecan-induced arthritis: a murine autoimmune mode/ of rheumatoid arthritis[J]. Methods Mol Med, 2004,102.. 313-338.
  • 8Ishikawa L L, Colavite P M, da Rosa L C,Balbino B, Franca T G, Zorzella-Pezavento S F, et al. Commercial bovine proteoglycan is highly arthritogenic and can be used as an alternative antigen source for PGIA model [J]. Biomed Res Int, 2014,2014 .. 148594.
  • 9Giant T T, Cs-Szab6 G, Nagase H, Jacobs J J, Mikecz K. Progressive polyarthritis induced in BALB/e mice by aggrecan from normal and osteoarthritic human car- tilage[J]. Arthritis Rheum, 1998,41 : 1007-1118.
  • 10Lark M W, Bayne E K, Flanagan J, Harper C F, Ho- errner L A, Hutchinson N I, et al. Aggrecan degrada- tion in human cartilage. Evidence for both matrix met- alloproteinase and aggrecanase activity in normal, os- teoarthritic, and rheumatoid joints[J]. J Clin Invest, 1997,100..93-106.

同被引文献82

引证文献6

二级引证文献30

第二军医大学学报
2015年 第5期

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部