期刊文献+

类风湿关节炎发病不同时期cDC成熟状态研究

Study on cDC maturation at different stages of rheumatoid arthritis
下载PDF
导出
摘要 目的采用hGPI325-339和hGPI469-483混合多肽片段构建类风湿关节炎(rheumatoid arthritis,RA)小鼠模型,观测RA小鼠体内经典树突状细胞(conventional dendritic cells,cDC)的频率及成熟状态。方法流式细胞术检测RA模型小鼠发病时脾脏、淋巴结cDC的频率和CD80、CD86分子的表达情况。结果RA小鼠脾脏cDC频率在炎症4个时期均显著低于健康对照组;CD80分子的表达在炎症初期、高峰期和缓解期明显高于健康对照组,在炎症进展期明显低于健康对照组;CD86分子的表达在炎症的4个时期均明显高于健康对照组。淋巴结cDC频率在炎症4个时期均显著高于健康对照组;CD80分子的表达在炎症初期明显高于健康对照组,其余3个时期均低于健康对照组;CD86分子的表达在炎症初期、进展期和缓解期明显低于健康对照组,在炎症高峰期高于健康对照组。结论在RA发生中脾脏cDC的抗原提呈作用较之淋巴结可能更为重要;RA中脾脏和淋巴结cDC的成熟度存在先升高后降低的起伏波动现象。 Objective To establish a mouse model of RA with hGPI325-339 and hGPI469-483 mixed peptides and observe the frequency and mature status of cDC in RA mice.Methods The frequency of cDC and the expression of CD80 and CD86 in spleen and lymph nodes of RA model mice were detected by flow cytometry.Results The frequency of cDC in spleen of RA mice was significantly lower than that of normal control group during the four stages of inflammation.The expression of CD80 was significantly higher than normal control group in the initial stage,peak stage and remission stage of inflammation,and was significantly lower than normal control group in the progressive stage of inflammation.The expression of CD86 was significantly higher than normal control group in all four stages of inflammation.The frequency of cDC in lymph nodes was significantly higher than normal control group in all four stages of inflammation.The expression of CD80 was significantly higher than normalcontrol group at the initial stage of inflammation and lower than normal control group at other three stages.The expression of CD86 was significantly lower than normal control group in the initial,progressive and remission stages of inflammation,and higher than normal control group in the peak of inflammation.Conclusion The antigen presenting role of splenic cDC may be more important than that of lymph nodes in RA.The cDC maturity of spleen and lymph node in RA show a fluctuating phenomenon that increases at first and then decreases.
作者 滕景芳 陈胜德 梁蕊 徐文斌 孟明 TENG Jingfang;CHEN Shengde;LIANG Rui;XU Wenbin;MENG Ming(School of Basic Medical Sciences,Hebei University,Baoding 071000,China;Key Laboratory of Pathogenesis Mechanism and Control of Inflammatory-Autoimmune Diseases of Hebei Province,Baoding 071000,China)
出处 《医学研究与教育》 CAS 2021年第4期1-7,共7页 Medical Research and Education
基金 国家自然科学基金面上项目(81771755)。
关键词 类风湿关节炎 CDC CD80 CD86 rheumatoid arthritis(RA) cDC CD80 CD86
  • 相关文献

参考文献1

二级参考文献15

  • 1Lee DM, Weinblatt ME. Rheumatoid arthritis[ J]. Lan- cet, 2001, 358(9285) :903-911.
  • 2Sehurgers E, Billiau A, Matthys P. Collagen-induced ar- thritis as an animal model for rheumatoid arthritis: focus on interferon-",/[J]. Interferon Cytokine Res, 2011, 31 (12) :917-926.
  • 3Griffiths MM, Returners EF. Genetic analysis of collagen- induced arthritis in rats: a polygenic model for rheumatoid arthritis predicts a common framework of cross-species in- flammatory/autoimmtme disease loci [ J 5. Immunol Rev, 2001, 184( 1 ) : 172-183.
  • 4van Haalen HG, Severens JL, Tran-Duy A, et al. How to select the right cost-effectiveness model? A systematic re- view and stepwise approach for selecting a transferable health economic evaluation model for rheumatoid arthritis [ J ]. Pharmacoeconomics, 2014, 32 (5) :429 442.
  • 5Schubert D, Maier B, Morawietz L, et al. Immunization with glucose-6-phosphate isomerase induces T cell-depen- dent peripheral polyarthritis in generally unaltered mice [J]. J Immunol, 2004, 172(7):4503-4509.
  • 6Horikoshi M, Goto D, Segawa S, et al. Activation of in- variant NKT cells with glyeolipid ligand a-galactosylceram- ide ameliorates glueose-6-phosphate isomerase peptide-in- duced arthritis[J]. PLoS One, 2012, 7(12) :e51215.
  • 7Bruns L, Frey O, Morawietz L, et al. Immunization with an immunodominant self-peptide derived from g|ucose-6- phosphate isomerase induces arthritis in DBA/1 mice[J]. Arthritis Res Ther, 2009, 11 (4) : R117.
  • 8Boissier MC, Assier E, Falgarone G, et al. Shifting the imbalance from Thl/Th2 to Thl7/treg: the changing rheu- matoid arthritis paradigm[ J]. Joint Bone Spine, 2008, 75 (4) :373-375.
  • 9Matsuda JL, Mallevaey T, Scott-Browne J, et al. CDld- restricted iNKT cells, 'the swiss-army knife' of the im- mune system [ J ]. Curt Opin Immunol, 2008, 20 (3) : 358-368.
  • 10Parietti V, Chiffiot 14, Sibilia J, et al. Rituximab treatment overcomes reduction of regulatory iNKT cells in patients with rheumatoid arthritis [ J ]. Clin Immunol, 2010, 134 (3) :331-339.

共引文献4

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