Class I and II histone deacetylase inhibition by ITF2357 reduces SLE pathogenesis in vivo.
Class I and II histone deacetylase inhibition by ITF2357 reduces SLE pathogenesis in vivo.
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ITF2357 抑制 I 类和 II 类组蛋白脱乙酰酶可减少体内 SLE 发病机制。
DOI：
10.1016/j.clim.2014.01.002
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发表时间：
2014-03
期刊：
影响因子：
--
通讯作者：
Reilly CM
中科院分区：
文献类型：
--
作者：
Regna NL;Chafin CB;Hammond SE;Puthiyaveetil AG;Caudell DL;Reilly CM
我们试图确定一种特定的I类和II类HDAC抑制剂（ITF 2357）是否能够通过调节T细胞谱来减少狼疮易感NZB/W小鼠的疾病。从22 - 38周龄开始，用ITF 2357（5 mg/kg或10 mg/kg）或媒介物对照处理NZB/W和非狼疮NZW小鼠。每2周测量一次体重和蛋白尿，每4周测量一次血清抗dsDNA和细胞因子水平。通过血清IgG水平、免疫复合物沉积和肾脏病理来确定肾脏疾病。采用流式细胞术分析评估T淋巴细胞特征。我们的结果显示，用高剂量ITF 2357处理的NZB/W小鼠具有降低的肾脏疾病和血清中的炎性细胞因子。用ITF 2357处理降低了Th 17表型，同时增加了Tcl 3的百分比以及Foxp 3乙酰化。这些结果表明，特异性HDAC抑制可以通过改变T细胞分化和乙酰化来减轻疾病。
We sought to determine if a specific class I and II HDAC inhibitor (ITF2357) was able to decrease disease in lupus-prone NZB/W mice through regulation of T cell profiles. From 22 - 38 weeks-of-age, NZB/W and non-lupus NZW mice were treated with ITF2357 (5 mg/kg or 10 mg/kg), or vehicle control. Body weight and proteinuria were measured every 2 weeks, while sera anti-dsDNA and cytokine levels were measured every 4 weeks. Kidney disease was determined by sera IgG levels, immune complex deposition, and renal pathology. T lymphocyte profiles were assessed using flow cytometric analyses. Our results showed NZB/W mice treated with the high-dose of ITF2357 had decreased renal disease and inflammatory cytokines in the sera. Treatment with ITF2357 decreased the Th17 phenotype while increasing the percentage of Tregs as well as Foxp3 acetylation. These results suggest that specific HDAC inhibition may decrease disease by altering T cell differentiation and acetylation.
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影响因子：
13.6
作者：
Crispín JC;Liossis SN;Kis-Toth K;Lieberman LA;Kyttaris VC;Juang YT;Tsokos GC
通讯作者：
Tsokos GC
影响因子：
5.3
作者：
Joshi, Sneha;Pantalena, Luiz-Carlos;Youssef, Sawsan
通讯作者：
Youssef, Sawsan
DOI：
10.1111/j.0959-9673.2005.00438.x
发表时间：
2005-10-01
影响因子：
3
作者：
Hayashi, T;Hasegawa, K;Adachi, C
通讯作者：
Adachi, C
影响因子：
5.7
作者：
Christensen, Dan P.;Dahllof, Mattias;Mandrup-Poulsen, Thomas
通讯作者：
Mandrup-Poulsen, Thomas
影响因子：
6.1
作者：
Hayashi, Toshiharu;Hasegawa, Keiko;Maeda, Ken
通讯作者：
Maeda, Ken