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[特应性皮炎的免疫发病机制]

[Immunopathogenesis of atopic eczema].

作者信息

Bjerke J R

机构信息

Hudavdelingen Medisinsk klinikk, Ullevål sykehus, Oslo.

出版信息

Tidsskr Nor Laegeforen. 1994 Jun 20;114(16):1827-8.

PMID:8079299
Abstract

The role of elevated serum IgE in patients with atopic eczema has been unclear. It has recently been shown that antigens from house dust mites may penetrate the skin, bind to IgE on Langerhans' cells, which in turn mediate the activation of antigen-specific TH2 cells that are the predominant T cells found in early atopic skin lesions. TH2 cells produce IL-4, which stimulates the IgE production by B lymphocytes, and are chemotactic for eosinophilic granulocytes. The discovery of microbial superantigens that activate T cells more easily and less specifically than the traditional antigens do, helps us to understand how local microbial agents can provoke the outburst of new atopic skin lesions.

摘要

血清IgE升高在特应性皮炎患者中的作用一直不明确。最近有研究表明,屋尘螨抗原可能穿透皮肤,与朗格汉斯细胞上的IgE结合,进而介导抗原特异性TH2细胞的激活,而TH2细胞是早期特应性皮肤病变中主要的T细胞。TH2细胞产生IL-4,刺激B淋巴细胞产生IgE,并对嗜酸性粒细胞具有趋化作用。微生物超抗原比传统抗原更易且更非特异性地激活T细胞,这一发现有助于我们理解局部微生物因子如何引发新的特应性皮肤病变的爆发。

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