Abstract
We thank Xu et al for their interest in our work on the role of EZH2 in lupus. We previously reported changes in T cell DNA methylation patterns that are associated with increased disease activity in lupus patients, and identified a possible role for EZH2 in inducing these pro-inflammatory epigenetic changes (1, 2). We followed this by mechanistic work in vitro that resulted in the identification of junctional adhesion molecule A (JAM-A) as a novel important target gene dysregulated by EZH2 in lupus T cells (3).
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