作者: Brian P. Lipsky , Dean Y. Toy , David A. Swart , Molly D. Smithgall , DirkE. Smith
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摘要: IL-33 signals through ST2, which is expressed either as a full-length signaling receptor or truncated soluble that can suppress activity. Previous data suggest ST2 mRNA in fibroblasts coupled to serum-inducible proximal promoter, while expression immune cells directed from distal promoter. In order better understand the function of alternative promoters and how they ultimately affect regulation IL-33, we generated mouse promoter deleted. Promoter deletion had no impact on mast their ability respond IL-33. contrast, it resulted complete loss both fibroblasts, corresponded with an inability secrete defect responsiveness. Importantly, spite fibroblast defect, concentrations were not reduced serum naive allergen-exposed knockout mice. summary, found usage largely cell-type dependent but does dictate splicing. Moreover, major driver circulating under conditions tested.