CD4+FOXP3+ T regulatory cells in human autoimmunity: more than a numbers game.
CD4+FOXP3+ T regulatory cells in human autoimmunity: more than a numbers game.
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DOI：
10.4049/jimmunol.1003224
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发表时间：
2011-09-01
期刊：
影响因子：
--
通讯作者：
Buckner JH
中科院分区：
文献类型：
--
作者：
Long SA;Buckner JH
调节性T细胞在自身免疫病理的抑制中起主导作用，因为在模型系统中拯救Treg数量和/或功能可以预防和逆转疾病。这些发现引发了一系列关于Treg数量和功能缺陷在人类自身免疫中的作用的研究。然而，证明被诊断患有自身免疫性疾病的个体Treg的整体缺陷一直具有挑战性。这些挑战部分是由于人类自身免疫性疾病的复杂性，其中各种遗传因素和环境触发因素导致疾病易感性，Treg介导的抑制失败对疾病发病机制的贡献可以扩展到多种机制。在这里，我们讨论了CD4+FOXP3+ Treg在人类自身免疫中的数量和功能，重点讨论了具有代表性的自身免疫性疾病，其中存在多种Treg介导的缺陷，并强调需要更好地了解Treg在自身免疫中的可塑性和功能。
Regulatory T cells play a dominant role in suppression of autoimmune pathology, as rescue of Treg number and/or function in model systems can both prevent and reverse disease. These findings have generated a series of studies addressing the role of defects in Treg number and function in human autoimmunity. However, demonstrating global defects in Treg of individuals diagnosed with autoimmune diseases has been challenging. These challenges are founded, in part, in the complexity of human autoimmune diseases in which various genetic factors and environmental triggers contribute to disease susceptibility and the contribution of failed Treg mediated suppression to the pathogenesis of disease can extend to multiple mechanisms. Here, we discuss what is known with respect to the number and function of CD4+FOXP3+ Treg in human autoimmunity, focusing on representative autoimmune diseases in which there are diverse Treg-mediated defects and highlight the need to better understand Treg plasticity and function in the context of autoimmunity.
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DOI：
10.1159/000289201
发表时间：
2010
期刊：
Current directions in autoimmunity
影响因子：
--
作者：
Chen X;Oppenheim JJ
通讯作者：
Oppenheim JJ
影响因子：
20.3
作者：
Borsellino, Giovanna;Kleinewietfeld, Markus;Falk, Kirsten
通讯作者：
Falk, Kirsten
影响因子：
2.7
作者：
Chistiakov, Dimitry A.;Chistiakov, Alexander P.
通讯作者：
Chistiakov, Alexander P.
影响因子：
7.7
作者：
Brusko, TM;Wasserfall, CH;Atkinson, MA
通讯作者：
Atkinson, MA
影响因子：
4.4
作者：
Fritzsching, B;Oberle, N;Suri-Payer, E
通讯作者：
Suri-Payer, E