The IL-2/IL-2R system: from basic science to therapeutic applications to enhance immune regulation.
The IL-2/IL-2R system: from basic science to therapeutic applications to enhance immune regulation.
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DOI：
10.1007/s12026-013-8452-5
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发表时间：
2013-12
影响因子：
4.4
通讯作者：
Malek, Thomas R.
中科院分区：
文献类型：
--
作者：
Bayer, Allison L.;Pugliese, Alberto;Malek, Thomas R.
IL-2在免疫系统的正常功能中起着至关重要的作用。作为淋巴细胞的营养因子，IL-2是建立和维持适应性T细胞反应所必需的；然而，IL-2也通过其对调节性T细胞（Treg细胞）的作用对免疫调节至关重要。多年来，我们对IL-2的生物学及其通过IL-2受体的信号传导的理解做出了贡献，并帮助确定了IL-2在Treg发育和功能中的关键作用。我们的数据表明Treg细胞对IL-2具有更高的敏感性，这可能为通过选择性刺激Treg细胞促进免疫调节创造了一个治疗窗口。我们现在正在努力将这些知识转化为临床领域，通过我们对1型糖尿病作为一种原型自身免疫性疾病的关注。具体来说，我们的目标是开发基于il -2的治疗方案，并结合增强抗原特异性Treg反应的手段，以改善和更有选择性地调节胰岛自身免疫。同时，我们正在研究自身免疫和移植的临床前模型，以确定成功的过继性Treg治疗的关键因素，并制定临床适用的治疗方案。
IL-2 plays a critical role in the normal function of the immune system. A trophic factor for lymphocytes, IL-2 is required for mounting and sustaining adaptive T cell responses; however, IL-2 is also critical for immune regulation via its effects on regulatory T cells (Treg cells). Over the years, we have contributed to the understanding of the biology of IL-2 and its signaling through the IL-2 receptor and helped define the key role played by IL-2 in Treg development and function. Our data show that Treg cells have a heightened sensitivity to IL-2, which may create a therapeutic window to promote immune regulation by selective stimulation of Treg cells. We are now developing new efforts to translate this knowledge to the clinical arena, through our focused interest in Type 1 diabetes as a prototypic autoimmune disease. Specifically, we aim at developing IL-2-based therapeutic regimens and incorporate means to enhance antigen-specific Treg responses, for improved and more selective regulation of islet autoimmunity. In parallel, we are pursuing studies in preclinical models of autoimmunity and transplantation to define critical factors for successful adoptive Treg therapy and develop clinically applicable therapeutic protocols.
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影响因子：
4.4
作者：
Burchill, Matthew A.;Yang, Jianying;Farrar, Michael A.
通讯作者：
Farrar, Michael A.
影响因子：
7.3
作者：
Akiyama T;Shinzawa M;Qin J;Akiyama N
通讯作者：
Akiyama N
影响因子：
15.3
作者：
Bayer, AL;Yu, AX;Adeegbe, D;Malek, TR
通讯作者：
Malek, TR
DOI：
10.4049/jimmunol.181.1.225
发表时间：
2008-07-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bayer AL;Lee JY;de la Barrera A;Surh CD;Malek TR
通讯作者：
Malek TR
影响因子：
56.9
作者：
Anderson, MS;Venanzi, ES;Mathis, D
通讯作者：
Mathis, D