首页> 外文期刊>The Journal of Allergy and Clinical Immunology >Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells
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Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells

机译:晚期糖基化终产物的肺受体通过IL-33和2型先天淋巴样细胞的积累促进哮喘发病

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摘要

Background: Single nucleotide polymorphisms in the human gene for the receptor for advanced glycation end-products (RAGE) are associated with an increased incidence of asthma. RAGE is highly expressed in the lung and has been reported to play a vital role in the pathogenesis of murine models of asthma/allergic airway inflammation (AAI) by promoting expression of the type 2 cytokines IL-5 and IL-13. IL-5 and IL-13 are prominently secreted by group 2 innate lymphoid cells (ILC2s), which are stimulated by the proallergic cytokine IL-33.
机译:背景:人类基因中晚期糖基化终产物(RAGE)受体的单核苷酸多态性与哮喘的发病率增加有关。 RAGE在肺中高表达,并且据报道通过促进2型细胞因子IL-5和IL-13的表达,在哮喘/过敏性气道炎症(AAI)鼠模型的发病中起着至关重要的作用。 IL-5和IL-13由第2组先天性淋巴样细胞(ILC2)显着分泌,其由前过敏性细胞因子IL-33刺激。

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