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首页> 外文期刊>Allergy >Intestinal epithelial cells express galectin-9 in patients with food allergy that plays a critical role in sustaining allergic status in mouse intestine.
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Intestinal epithelial cells express galectin-9 in patients with food allergy that plays a critical role in sustaining allergic status in mouse intestine.

机译:食物过敏患者的肠上皮细胞表达galectin-9,其在维持小鼠肠道过敏状态中起关键作用。

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BACKGROUND AND AIMS: Mechanisms in sustaining the allergic hypersensitivity status in the body are unclear. Galectin-9 (Gal-9) has strong immune regulatory capacity. The present study aims to elucidate the role of Gal-9 in sustaining allergic status in the intestine. METHODS: Duodenal biopsies were obtained from 20 patients with peptic ulcer and food allergy (FA). The expression of Gal-9 in intestinal tissue was examined at both protein level and mRNA level. Two coculture systems with intestinal epithelial cells (IEC) and mast cells, or dendritic cells (DC) and T cells were established to investigate the source of Gal-9 in the intestine and the mechanism by which Gal-9 modulated DC's phenotyping and sustained the T helper 2 polarization. RESULTS: Normal IEC showed mild expression of Gal-9 that was markedly enhanced in patients with FA. Mast cells had the capability to induce IEC to produce Gal-9 via releasing tryptase that activated the proteinase-activated receptor 2 on IEC. Gal-9 activated DC to produce TIM4 (T-cell immunoglobulin mucin domain) via ligating TIM3 on DC via activating the cyclic guanosine monophosphate (cGMP) pathway. In a mouse FA model, blocking Gal-9 inhibited the allergic hypersensitivity status and the antigen-specific Th2 response in the intestine. CONCLUSIONS: IEC-derived Gal-9 contributes to sustaining the allergic status in the intestine.
机译:背景和目的:维持体内过敏性超敏反应状态的机制尚不清楚。 Galectin-9(Gal-9)具有很强的免疫调节能力。本研究旨在阐明Gal-9在维持肠道过敏状态中的作用。方法:对20例消化性溃疡和食物过敏(FA)患者进行十二指肠活检。在蛋白质水平和mRNA水平上检查了Gal-9在肠组织中的表达。建立了两个具有肠道上皮细胞(IEC)和肥大细胞,或树突状细胞(DC)和T细胞的共培养系统,以研究肠道中Gal-9的来源以及Gal-9调节DC表型并维持DC的机制。 T辅助2极化。结果:正常IEC显示Gal-9的轻度表达,在FA患者中明显增强。肥大细胞具有通过释放激活IEC上的蛋白酶激活受体2的类胰蛋白酶来诱导IEC产生Gal-9的能力。 Gal-9通过激活环鸟苷单磷酸(cGMP)途径将TIM3连接到DC,从而激活DC以产生TIM4(T细胞免疫球蛋白粘蛋白结构域)。在小鼠FA模型中,阻断Gal-9抑制了肠道的过敏性超敏反应状态和抗原特异性Th2反应。结论:IEC衍生的Gal-9有助于维持肠道的过敏状态。

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