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W e read with interest the recent paper by Larsen and colleagues (1), in which the authors elegantly identify a regulatory region within the first intron of Foxn1 that is essential for the expression of this transcription factor within thymic epithelial cells (TEC). The authors further suggest that binding of several candidate transcription factors could modulate Foxn1 expression. Because there is convincing evidence that Foxn1 expression may be controlled by an autoregulatory mechanism (2, 3), we interrogated our TEC-specific FOXN1 chromatin immunoprecipitation sequencing (ChIP-seq) dataset for a FOXN1 binding site within the first intron of Foxn1 (4). This identified a significant FOXN1 ChIP-seq peak (irreproducibility discovery rate , 0.05) within the region described by Larsen and colleagues (Fig. 1). There was a canonical FOXN1binding motif (GACGC) located near the summit of the FOXN1 ChIP-seq peak. We therefore suspect that some of the deficiency in FOXN1 expression observed by the authors following the genetic ablation of this regulatory element may be secondary to the loss of autoregulatory Foxn1 expression. FOXN1 is expressed in TEC and epithelia of the skin (5). Chromatin accessibility determined by other transcription factor pathways and epigenetic mechanisms may establish tissue-specific gene expression profiles in these two tissues. Understanding this mechanism could have implications for the in vitro generation of TEC and their future therapeutic use for the correction of immunodeficiency and autoimmunity. Adam E. Handel and Georg A. Holländer

Comment on “Identification of an Intronic Regulatory Element Necessary for Tissue-Specific Expression of Foxn1 in Thymic Epithelial Cells”