期刊文献+

间充质干细胞在结核分枝杆菌感染免疫反应中的作用研究进展 被引量:1

Advances in the effects of mesenchymal stem cells on immune response during Mycobacterium tuberculosis infection
原文传递
导出
摘要 结核病(TB)每年导致200多万人死亡,在全球单一传染病死亡率中位居第二。尽管宿主产生了强大的免疫反应,但结核分枝杆菌(MTB)还是成功地逃避了宿主的免疫,并建立了一个持续性感染的状态。MTB以何种机制逃避有力的宿主免疫反应仍不完全清楚。有研究证实间充质干细胞(MSCs)参与了宿主抗MTB的免疫反应。MTB通过招募MSCs到达感染部位来抑制T细胞的免疫反应。MSCs渗入感染MTB的小鼠组织和T淋巴细胞中,参与肉芽肿的形成,诱导Tregs的分化和发育及建立T细胞耐受。MSCs可通过产生一氧化氮(NO)来抑制T细胞的免疫反应,及影响TGF-β受体Ⅱ的功能来增加TB的易感性。MSCs在MTB逃避宿主的免疫反应中起着重要的作用,有望成为TB治疗的独特靶点。 Tuberculosis(TB) is the cause of 2 million deaths each year and is the second largest cause of mortality from a single infectious disease worldwide.Despite production of a robust host immune response,Mycobacterium tuberculosis(MTB)successfully evades host immunity and establishes a persistent infection.The mechanism by which MTB evades the host’s robust immune response is still not fully understood.Studies have confirmed that mesenchymal stem cells(MSCs) are involved in a host’s immune response to MTB.MTB suppresses T-lymphocyte responses by recruiting MSCs to the site of infection.MSCs infiltrate tissues in mice and T-lymphocytes are involved in granuloma formation,induction of Tregs differentiation,and development and establishment of T cell tolerance.MSCs suppress T-cell responses by producing nitric oxide and increasing the susceptibility to tuberculosis by affecting TGF-β receptor Ⅱ function.MSCs play an important role in MTB’s evasion of the host’s immune response and should become a unique target for treatment of TB.
作者 黄艺 袁俐
出处 《中国病原生物学杂志》 CSCD 北大核心 2012年第8期629-631,640,共4页 Journal of Pathogen Biology
基金 国家自然科学基金项目(No.30960356 No.81160368)
关键词 MTB 间充质干细胞 免疫抑制 综述 Mycobacterium tuberculosis; mesenchymal stem cells; immunosuppression; review
  • 相关文献

参考文献3

二级参考文献66

  • 1周官恩,刘宗超,王宇石,饶明俐.p38丝裂原活化蛋白激酶与缺血性脑损伤[J].中风与神经疾病杂志,2004,21(5):473-475. 被引量:4
  • 2杜宏举,汤宁.丝裂原活化蛋白激酶信号通路及其生物学功能[J].国外医学(卫生学分册),2005,32(4):197-201. 被引量:12
  • 3Mehdi Mohamadnejad,Mehrnaz Namiri,Mohamad Bagheri,Seyed Masiha Hashemi,Hossein Ghanaati,Narges Zare Mehrjardi,Saeed Kazemi Ashtiani,Reza Malekzadeh,Hossein Baharvand.Phase 1 human trial of autologous bone marrow-hematopoietic stem cell transplantation in patients with decompensated cirrhosis[J].World Journal of Gastroenterology,2007,13(24):3359-3363. 被引量:76
  • 4Robert AB, Anzano MA, Lamb LC, et al. New class of transforming growth factors potentiated by epidermal growth factor:isolation from non-neoplastic tissues[ J]. Proc Natl Acad Sci U S A, 1981,78 (9) :5339-5343.
  • 5Brown JD,DiChiara MR, Anderson KR, et al. MEKK-1, a component of the stress( stress-activated protein kinase/c-Jun N-terminal kinase) pathway, can selectively activate Smad2-mediated transcriptional activation in endothelial cells [J].J Biol Chem, 1999, 247 ( 13 ) :8797-8805.
  • 6Atfi A, Djelloul S, Chastre E,et al. Evidence for a role of Rho-like GTPases and stress-activated protein kinase/c-Jun N-terminal kinase(SAPK/JNK) in transforming growth factor beta-mediated signaling[ J ]. J Biol Chem, 1997,272 (3) : 1429-1432.
  • 7Hocevar BA, Brown TL, Howe PH. TGF-beta induces fibronectin synthesis through a c-Jun N-terminal kinase-dependent, Smad4-independent pathway [ J ]. EMBO J, 1999,18 ( 5 ) : 1345-1356.
  • 8Baardsnes J, Hinck CS, Hinck AP, et al. TbetaR- 1I discriminates the high-and low-affinity TGF-beta isoforms via two hydrogenbonded ion pairs[J]. Biochemistry,2009,48(10) :2146-2155.
  • 9Cutroneo KR. TGF-beta-induced fibrosis and SMAD signaling: oligo decoys as natural therapeutics for inhibition of tissue fibrosis and scarring[ J]. Wound Repair Regen ,2007,15 ( Suppl 1 ) : S54-S60. Massague J. TGF-beta in cancer [ J]. Cell, 2008, 134 (2): 215-230.
  • 10Massague J. TGF-beta in cancer[J]. Cell, 2008, 134 (2): 215-230.

共引文献93

同被引文献4

引证文献1

二级引证文献2

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