pmid:
t helper (th)-cell subsets, such as th1 and th17, mediate inflammation in both peripheral tissues and central nervous system. here we show that stat5 is required for t helper-cell pathogenicity in autoimmune neuroinflammation but not in experimental colitis. although stat5 promotes regulatory t cell g手术治多发性硬化症eneration and immune suppression, loss of stat5 in cd4+ t cells resulted in diminished development of experimental autoimmune encephalomyelitis (eae), a mouse model of multiple sclerosis. our results showed that loss of encephalitogenic activity of stat5-deficient autoreactive cd4+ t cells was independent多发性硬化mri of ifn-γ or interleukin 17 (il-17) production, but was due to the impaired expression of granulocyte-macrophage colony-stimulating factor (gm-csf), a crucial mediator of t-cell pathogenicity. we further showed that il-7-activated stat5 promotes the generation of gm-csf-producing cd4+ t cells, which were prefe多发性硬化护理诊断rentially able to induce more severe eae than th17 or th1 cells. consistent with gm-csf-producing cells being a distinct subset of th cells, the differentiation program of these cells was distinct from that of th17 or th1 cells. we further found that il-3 was secreted in a similar pattern as gm-csf in this治疗多发性硬化症的医院 subset of th cells. in conclusion, the il-7-stat5 axis promotes the generation of gm-csf/il-3-producing th cells. these cells display a distinct transcriptional profile and may represent a novel subset of t helper cells which we designate as th-gm.
wanqiang sheng1,2, fan yang1, yi zhou3, henry yang1, pey yn多发性硬化的治疗g low4, david michael kemeny4, patrick tan1,5, akira moh7, mark h kaplan7,8, yongliang zhang4 and xin-yuan fu1,3,6,8
doi:10.1038/cr.2014.154
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研究人员在1992年时发现了stat蛋白家族及其名为jak-stat信号通路,感染该路径可以引发许多类型的炎性疾病;如今研究者发现干扰jak-stat信号通路的的药物可以治疗许多疾病;而il-7/stat5的发现在神经炎性疾病领域可以增加研究人员对药物的开发及新型疗法的研究最后研究人员希望对th-gm的生理功能的理解或将帮多发性硬化的危害助开发治疗多种人类自身免疫疾病的新型疗法(生物谷bioon.com)
pmc:
研究者xin-yuan fu教授表示,我们发现了一种名为th-gm的新型免疫辅助t细胞,其在免疫系统和神经炎症的发病机制中扮演着重要角色,该项研究为开发新型干预疗法来帮助治疗多发性硬化症非常关键一种stat家族蛋白成员stat5蛋白可以指挥th-gm来开启对自身抗原的免疫反应从而对白细胞介素il-7作出反应,进而引发中枢神经系统的神经炎性、发病及损伤;阻断il-7或stat5获将为治疗疾病带来新的思路
ms是个体中枢神经系统常见的一种自身免疫疾病,其在全球影响着250万人的健康,而且在北欧地区广为流行,尽管研究者进行了这么多年的研究,但是晚期多发性硬化ms的发病机制依然尚不清楚,而且该疾病也很难治愈而本文研究中研究者揭示了il-7/stat5介导的信号通路和t辅助细胞介导的病理机制之间的紧密关联谢谢!
stat5 programs a distinct subset of gm-csf-producing t helper cells that is essential for autoimmune neuroinflammation
2014年11月26日 讯 /生物谷bioon/ --近日,一篇发表在国际杂志cell research上的研究论文中,来自新加坡国立大学的研究人员进行了一项多领域的研究发现了一种新型的免疫细胞,这种免疫细胞或可以帮助有效改善多发性硬化多发性硬化症怎么治疗好症(ms)的治疗效果
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