IL-2 family cytokines: new insights into the complex roles of IL-2 as a broad regulator of T helper cell differentiation.
IL-2 family cytokines: new insights into the complex roles of IL-2 as a broad regulator of T helper cell differentiation.
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DOI：
10.1016/j.coi.2011.08.003
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发表时间：
2011-10
影响因子：
7
通讯作者：
Leonard WJ
中科院分区：
文献类型：
--
作者：
Liao W;Lin JX;Leonard WJ
白细胞介素-2（IL-2）是一种多效性细胞因子，其驱动T细胞生长，增强NK细胞溶解活性，诱导调节性T细胞的分化，并介导活化诱导的细胞死亡。IL-2与IL-4、IL-7、IL-9、IL-15和IL-21沿着共享共同的细胞因子受体γ链γ c，其在患有X连锁严重联合免疫缺陷的人类中突变。在此，我们主要集中在最近发现的IL-2在广泛调节T细胞的T辅助细胞分化的复杂作用。IL-2不指定发生的Th分化的类型;相反，IL-2调节其他细胞因子和转录因子的受体的表达，从而促进或抑制与每个Th分化状态相关的细胞因子级联。以这种方式，IL-2可以引发并潜在地维持Th1和Th2分化以及扩增这样的细胞群，而它抑制Th17分化，但也可以扩增Th17细胞。
Interleukin-2 (IL-2) is a pleiotropic cytokine that drives T-cell growth, augments NK cytolytic activity, induces the differentiation of regulatory T cells, and mediates activation-induced cell death. Along with IL-4, IL-7, IL-9, IL-15, and IL-21, IL-2 shares the common cytokine receptor γ chain, γc, which is mutated in humans with X-linked severe combined immunodeficiency. Herein, we primarily focus on the recently discovered complex roles of IL-2 in broadly modulating T cells for T helper cell differentiation. IL-2 does not specify the type of Th differentiation that occurs; instead, IL-2 modulates expression of receptors for other cytokines and transcription factors, thereby either promoting or inhibiting cytokine cascades that correlate with each Th differentiation state. In this fashion, IL-2 can prime and potentially maintain Th1 and Th2 differentiation as well as expand such populations of cells, whereas it inhibits Th17 differentiation but also can expand Th17 cells.
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影响因子：
56.9
作者：
MORGAN, DA;RUSCETTI, FW;GALLO, R
通讯作者：
GALLO, R
影响因子：
64.5
作者：
BLACKMAN, MA;TIGGES, MA;KOSHLAND, ME
通讯作者：
KOSHLAND, ME
影响因子：
64.8
作者：
MACCHI, P;VILLA, A;NOTARANGELO, LD
通讯作者：
NOTARANGELO, LD
影响因子：
32.4
作者：
Bird, JJ;Brown, DR;Reiner, SL
通讯作者：
Reiner, SL
DOI：
10.1084/jem.189.6.969
发表时间：
1999-03-15
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Chang JT;Shevach EM;Segal BM
通讯作者：
Segal BM