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Soluble ST2 suppresses the effect of interleukin-33 on lung type 2 innate lymphoid cells

机译:可溶性ST2抑制白介素33对肺2型先天性淋巴样细胞的作用

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摘要

Type 2 innate lymphoid cells (ILC2) in lungs produce interleukin (IL)-5 and IL-13 in response to IL-33 and may contribute to the development of allergic diseases such as asthma. However, little is known about negative regulators and effective inhibitors controlling ILC2 function. Here, we show that soluble ST2, a member of the IL-1 receptor family, suppresses the effect of IL-33 on lung ILC2 in vitro. Stimulation with IL-33 to naïve ILC2 induced morphological change and promoted cell proliferation. In addition, IL-33 upregulated expression of cell surface molecules including IL-33 receptor and induced production of IL-5 and IL-13, but not IL-4. Pretreatment with soluble ST2 suppressed IL-33-mediated responses of ILC2. The results suggest that soluble ST2 acts as a decoy receptor for IL-33 and protects ILC2 from IL-33 stimulation.
机译:肺中的2型先天性淋巴样细胞(ILC2)响应IL-33产生白介素(IL)-5和IL-13,并可能有助于过敏性疾病的发展,例如哮喘。但是,关于负调节剂和控制ILC2功能的有效抑制剂知之甚少。在这里,我们表明可溶性ST2,IL-1受体家族的一员,在体外抑制IL-33对肺ILC2的作用。用IL-33刺激幼稚的ILC2可诱导形态变化并促进细胞增殖。此外,IL-33上调了包括IL-33受体在内的细胞表面分子的表达,并诱导了IL-5和IL-13(而非IL-4)的产生。用可溶性ST2预处理抑制IL-33介导的ILC2反应。结果表明可溶性ST2充当IL-33的诱饵受体,并保护ILC2免受IL-33的刺激。

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