EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #73852_C
JAK/STAT通路抑制剂；抑制STAT5
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总览
STAT5抑制剂是一种可渗透细胞的非羰基烟酰腙，通过结合STAT5的SH2结构域特异性抑制其功能 （IC₅₀ = 47 μ M）。它对STAT1、STAT3或LCK的SH2结构域的抑制作用减弱（Müller等人）。
免疫学
·高浓度下诱导成熟嗜酸性粒细胞部分凋亡（Schwartz et al.）。
·恢复部分再刺激的TH17克隆产生IL-17（Zielinski et al.）
·抑制体外诱导调节性T细胞（iTregs）的生长（Betts et al.）。
细胞类型
粒细胞及其亚群，T 细胞
种属
人，小鼠，非人灵长类，其他物种，大鼠
研究领域
免疫
CAS 编号
285986-31-4
化学式
C₁₆H₁₁N₃O₃
纯度
≥ 95 %
通路
JAK/STAT
靶点
STAT5
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相关材料与文献
技术资料 (1)
文献 (4)
Discovery of chromone-based inhibitors of the transcription factor STAT5.
Chembiochem : a European journal of chemical biology 2008 MAR
Abstract
Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β.
Nature 2012 APR
Abstract
IL-17-producing CD4+ T helper cells (TH17) have been extensively investigated in mouse models of autoimmunity. However,the requirements for differentiation and the properties of pathogen-induced human TH17 cells remain poorly defined. Using an approach that combines the in vitro priming of naive T cells with the ex vivo analysis of memory T cells,we describe here two types of human TH17 cells with distinct effector function and differentiation requirements. Candida albicans-specific TH17 cells produced IL-17 and IFN-γ,but no IL-10,whereas Staphylococcus aureus-specific TH17 cells produced IL-17 and could produce IL-10 upon restimulation. IL-6,IL-23 and IL-1β contributed to TH17 differentiation induced by both pathogens,but IL-1β was essential in C. albicans-induced TH17 differentiation to counteract the inhibitory activity of IL-12 and to prime IL-17/IFN-γ double-producing cells. In addition,IL-1β inhibited IL-10 production in differentiating and in memory TH17 cells,whereas blockade of IL-1β in vivo led to increased IL-10 production by memory TH17 cells. We also show that,after restimulation,TH17 cells transiently downregulated IL-17 production through a mechanism that involved IL-2-induced activation of STAT5 and decreased expression of ROR-γt. Taken together these findings demonstrate that by eliciting different cytokines C. albicans and S. aureus prime TH17 cells that produce either IFN-γ or IL-10,and identify IL-1β and IL-2 as pro- and anti-inflammatory regulators of TH17 cells both at priming and in the effector phase.
STAT5 polarization promotes iTregs and suppresses human T-cell alloresponses while preserving CTL capacity.
Journal of leukocyte biology 2014 FEB
Abstract
Alloreactivity negatively influences outcomes of organ transplantation or HCT from allogeneic donors. Standard pharmacologic immune suppression impairs T-cell function and jeopardizes the beneficial reconstitution of Tregs. Murine transplantation models have shown that STAT3 is highly expressed in alloreactive T cells and may be therapeutically targeted. The influence and effects of STAT3 neutralization in human alloreactivity,however,remain to be elucidated. In this study,S3I-201,a selective small-molecule inhibitor of STAT3,suppressed human DC-allosensitized T-cell proliferation and abrogated Th17 responses. STAT3 blockade significantly enhanced the expansion of potent iTregs and permitted CD8(+) cytolytic effector function. Mechanistically,S3I-201 polarized the ratio of STAT phosphorylation in favor of STAT5 over STAT3 and also achieved a significant degree of Foxp3 demethylation among the iTregs. Conversely,selective impairment of STAT5 phosphorylation with CAS 285986-31-4 markedly reduced iTregs. STAT3 represents a relevant target for achieving control over human alloresponses,where its suppression facilitates STAT5-mediated iTreg growth and function.
更多信息
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 285986-31-4 |
| Chemical Formula | C₁₆H₁₁N₃O₃ |
| 纯度 | ≥ 95 % |
| Target | STAT5 |
| Pathway | JAK/STAT |
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