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首页> 外文期刊>Allergy >Mast cells express IL-13Ralpha1: IL-13 promotes human lung mast cell proliferation and FcepsilonRI expression.
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Mast cells express IL-13Ralpha1: IL-13 promotes human lung mast cell proliferation and FcepsilonRI expression.

机译：肥大细胞表达IL-13Ralpha1：IL-13促进人肺肥大细胞增殖和FcepsilonRI表达。

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摘要

The Th2 cytokine interleukin (IL)-13 is implicated in the development of various allergic diseases including asthma. The IL-13 receptor, IL-13Ralpha1, is expressed on most leukocytes, except T-cells. Evidence to support IL-13Ralpha1 expression on mast cells is limited. We investigated: (i) IL-13Ralpha1 expression by human lung mast cells (HLMC); (ii) the number of IL-13Ralpha1+ bronchial submucosal mast cells in subjects with asthma and normal controls and (iii) the effect of IL-13 priming on HLMC expression of high-affinity IgE receptor (FcepsilonRI), stem cell factor receptor (CD117), histamine release, proliferation, and survival. Human lung mast cell expressed IL-13Ralpha1 mRNA. IL-13Ralpha1 was highly expressed on the surface HLMC (82 +/- 9%). Bronchial submucosal mast cell IL-13Ralpha1 expression was higher in asthmatics (86 +/- 2%) than normal controls (78 +/- 2%; P = 0.015). IL-13 priming for 30 min did not increase HLMC histamine release, in the presence or absence of SCF or in response to IgE/anti-IgE activation. IL-13 priming for 5 days upregulated HLMC FcepsilonRI expression (22% increase in fluorescent intensity; P = 0.003), increased histamine release following IgE/anti-IgE activation by 56% (P = 0.03) and increased proliferation by 50% (P = 0.003) without affecting cell survival or CD117 expression. The IL-13 specific neutralizing antibody CAT-354 inhibited all IL-13 mediated effects. Human lung mast cell express IL-13Ralpha1 and activation by IL-13 for 5 days increased FcepsilonRI expression and proliferation. Histamine release was not affected by short-term priming with IL-13, but was upregulated by priming for 5 days suggesting that this effect was mediated by the increased FcepsilonRI expression. These data support the view that targeting IL-13 may be beneficial in the treatment of asthma.
机译：Th2细胞因子白介素（IL）-13与包括哮喘在内的各种过敏性疾病的发展有关。 IL-13受体IL-13Ralpha1在除T细胞外的大多数白细胞中表达。支持肥大细胞上IL-13Ralpha1表达的证据有限。我们研究了：（i）人肺肥大细胞（HLMC）的IL-13Ralpha1表达; （ii）患有哮喘和正常对照的受试者中IL-13Ralpha1 +支气管黏膜下肥大细胞的数量，以及（iii）IL-13引发对高亲和力IgE受体（FcepsilonRI），干细胞因子受体（CD117）HLMC表达的影响），组胺的释放，增殖和生存。人肺肥大细胞表达IL-13Ralpha1 mRNA。 IL-13Ralpha1在表面HLMC上高表达（82 +/- 9％）。哮喘患者的支气管粘膜下肥大细胞IL-13Ralpha1表达高于正常对照组（78 +/- 2％; P = 0.015）。在存在或不存在SCF或响应IgE /抗IgE激活的情况下，IL-13引发30分钟不会增加HLMC组胺的释放。 IL-13启动5天可上调HLMC FcepsilonRI表达（荧光强度增加22％; P = 0.003），IgE /抗IgE激活后组胺释放增加56％（P = 0.03），增殖增加50％（P = 0.003），而不会影响细胞存活或CD117表达。 IL-13特异性中和抗体CAT-354抑制所有IL-13介导的作用。人肺肥大细胞表达IL-13Ralpha1，并被IL-13激活5天，增加FcepsilonRI表达和增殖。组胺的释放不受IL-13短期启动的影响，但通过启动5天而上调，表明该作用是由FcepsilonRI表达的增加介导的。这些数据支持以下观点：靶向IL-13可能对哮喘的治疗有益。

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