Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata 700054, India.
Department of Biophysics, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata 700054, India.
Immunity. 2013 Dec 12;39(6):1057-69. doi: 10.1016/j.immuni.2013.11.005. Epub 2013 Dec 5.
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the authors. This study provided an explanation for why loss of FoxP3 in inducible regulatory T cells results in reduced expression of interleukin (IL)-10 despite the absence of FoxP3 binding sites in the IL-10 promoter. STAT3 binding sites do exist in the promoter, and evidence for a direct molecular interaction between FoxP3 and STAT3 proteins was provided as an explanation of the effect of loss of FoxP3. As supporting evidence, we reported modeling of a structural interaction between these two transcription factors in Figure 4D. As the N-terminal region of FoxP3, which consists of the Exon-2 region, had not been solved at structural resolution, we mistakenly used what we deduced to be a FoxP3 related transcription factor, NFAT, in the modeling. The model depicted in Figure 4D therefore did not represent a putative interaction between FoxP3 and STAT3 as labeled, but rather a putative interaction between NFAT and STAT3. Given the incorrect labeling of Figure 4D, the lack of documentation in the paper describing exactly how the modeling was performed, the lack of evidence shown in the paper for the choice of NFAT as the modeling partner, and the limited supporting evidence for a cooperative interaction between FoxP3 and STAT3, the editors have concluded with the corresponding author that the appropriate course of action is to retract the paper. We apologize for any confusion and inconvenience caused to readers.
请参阅 Elsevier 撤稿政策(http://www.elsevier.com/locate/withdrawalpolicy)。应作者要求,本文已被撤回。该研究解释了为什么诱导型调节性 T 细胞中 FoxP3 的缺失导致白细胞介素(IL)-10 的表达降低,尽管 IL-10 启动子中不存在 FoxP3 结合位点。STAT3 结合位点确实存在于启动子中,并且提供了 FoxP3 和 STAT3 蛋白之间直接分子相互作用的证据,以解释 FoxP3 缺失的影响。作为支持证据,我们在图 4D 中报告了这两个转录因子之间结构相互作用的建模。由于 FoxP3 的 N 端区域(由外显子 2 区域组成)尚未以结构分辨率解决,因此我们在建模中错误地使用了我们推断为与 FoxP3 相关的转录因子 NFAT。因此,图 4D 中所示的模型并未代表所标记的 FoxP3 和 STAT3 之间的假定相互作用,而是代表 NFAT 和 STAT3 之间的假定相互作用。鉴于图 4D 的错误标记,论文中没有描述建模是如何进行的确切文档,论文中没有显示选择 NFAT 作为建模伙伴的证据,以及 FoxP3 和 STAT3 之间合作相互作用的有限支持证据,编辑们与相应的作者一起得出结论,采取的适当行动是撤回该论文。我们对给读者带来的任何困惑和不便表示歉意。