ArticleGenes and immunity2013
IL-2/IL-15 activate the human clonally restricted KIR3DL1 reverse promoter.
Article in Genes and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors at 2 institutions in 1 country.
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Abstract
Killer cell immunoglobulin-like receptors (KIRs) are expressed in a clonally restricted manner by human natural killer (NK) cells and allow detection of aberrant cells with low major histocompatibility complex class I levels. Clonally restricted KIR transcription is maintained by demethylation of the proximal promoter. Antisense transcripts also arise from this promoter and may enforce silencing of nonexpressed methylated KIR alleles in NK cells. Here we show that interleukin (IL)-2 and IL-15, cytokines critical for NK cell development and maintenance, greatly stimulated KIR3DL1 reverse promoter activity, but not forward promoter activity. Activated STAT5 was both necessary and sufficient for this effect and bound to the promoter in NK cells that expressed KIR3DL1 or were poised for expression. A systematic investigation of the KIR3DL1 reverse promoter showed significant differences from the forward promoter, with STAT and YY1 sites having relatively greater roles in regulating reverse proximal promoter activity. On the basis of our data, we propose a new role for antisense transcripts in the initiation of KIR gene expression during NK cell development.
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