Cytokine-induced monocyte characteristics in SLE.
Cytokine-induced monocyte characteristics in SLE.
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DOI：
10.1155/2010/507475
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发表时间：
2010
影响因子：
--
通讯作者：
Sullivan KE
中科院分区：
文献类型：
--
作者：
Zhang Z;Maurer K;Perin JC;Song L;Sullivan KE
SLE 中的单核细胞在许多检测中被描述为具有异常行为。我们检查了基因表达，并使用全基因组方法来研究翻译后组蛋白标记 H4 乙酰化，以检查 SLE 单核细胞的表观遗传变化。我们将 SLE 单核细胞基因表达和 H4 乙酰化与三种细胞因子处理的单核细胞进行比较，以了解哪种细胞因子作用在 SLE 单核细胞中占主导地位。我们发现 γ-干扰素和 α-干扰素都复制了 SLE 单核细胞中观察到的广泛基因表达变化。 SLE 单核细胞中的 H4 乙酰化总体高于对照，并且与基因表达比较时相比，H4ac 与细胞因子处理的细胞的相关性较小。一组趋化因子基因和 H4ac 表达下调。因此，SLE 中存在大量异常表达基因，这些基因与 H4ac 的改变密切相关，表明这些细胞的表观基因组经历了持久的变化。
Monocytes in SLE have been described as having aberrant behavior in a number of assays. We examined gene expression and used a genome-wide approach to study the posttranslational histone mark, H4 acetylation, to examine epigenetic changes in SLE monocytes. We compared SLE monocyte gene expression and H4 acetylation with three types of cytokine-treated monocytes to understand which cytokine effects predominated in SLE monocytes. We found that γ-interferon and α-interferon both replicated a broad range of the gene expression changes seen in SLE monocytes. H4 acetylation in SLE monocytes was overall higher than in controls and there was less correlation of H4ac with cytokine-treated cells than when gene expression was compared. A set of chemokine genes had downregulated expression and H4ac. Therefore, there are significant clusters of aberrantly expressed genes in SLE which are strongly associated with altered H4ac, suggesting that these cells have experienced durable changes to their epigenome.
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DOI：
10.1084/jem.20021553
发表时间：
2003-03-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bennett L;Palucka AK;Arce E;Cantrell V;Borvak J;Banchereau J;Pascual V
通讯作者：
Pascual V
DOI：
10.1073/pnas.88.9.3608
发表时间：
1991-05-01
影响因子：
11.1
作者：
BELLEFROID, EJ;PONCELET, DA;MARTIAL, JA
通讯作者：
MARTIAL, JA
影响因子：
2.6
作者：
Bengtsson, AA;Sturfelt, G;Rönnblom, L
通讯作者：
Rönnblom, L
影响因子：
158.5
作者：
Asanuma, Y;Oeser, A;Stein, CM
通讯作者：
Stein, CM
影响因子：
12.8
作者：
Amel-Kashipaz, MR;Huggins, ML;Powell, RJ
通讯作者：
Powell, RJ