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朗格汉斯细胞T6、DR及DQ抗原表达的调节:一种假说

The regulation of Langerhans cell T6, DR and DQ antigen expression: an hypothesis.

作者信息

Walsh L J, Seymour G J, Powell R N

机构信息

Department of Social and Preventive Dentistry, University of Queensland Dental School, Brisbane, Australia.

出版信息

J Oral Pathol. 1988 Jan;17(1):43-6. doi: 10.1111/j.1600-0714.1988.tb01504.x.

Abstract

A hypothetical model of the maturation pathway of Langerhans cells (LC) within an epithelial environment is presented. This model is based on in vitro studies using human gingival organ culture. In this model, T6 (CD1) antigen is induced on a T6(-) intraepithelial population by Interleukin-1 secreted by epithelial cells. This process is abrogated by a locally produced Interleukin-1 inhibitor, ILS. These T6(+) LC then express first HLA-DR and subsequently HLA-DQ surface antigens under the influence of either lipopolysaccharide or gamma interferon. The induction of these Class II antigens on LC is inhibited by prostaglandin E2. It is postulated that these Class II antigen positive LC are then available to function as antigen presenting cells. This hypothesis is consistent with in vitro studies and several in vivo observations. The basis of the hypothesis is the demonstration that locally produced factors may exert an influence on LC behaviour within an epithelial environment.

摘要

本文提出了一种朗格汉斯细胞(LC)在上皮环境中成熟途径的假设模型。该模型基于使用人牙龈器官培养的体外研究。在此模型中,上皮细胞分泌的白细胞介素-1可诱导T6(-)上皮内细胞群表达T6(CD1)抗原。这一过程可被局部产生的白细胞介素-1抑制剂ILS消除。这些T6(+)LC随后在脂多糖或γ干扰素的影响下首先表达HLA-DR,随后表达HLA-DQ表面抗原。前列腺素E2可抑制LC上这些II类抗原的诱导。据推测,这些II类抗原阳性的LC随后可作为抗原呈递细胞发挥作用。这一假设与体外研究和一些体内观察结果一致。该假设的基础是证明局部产生的因子可能会对上皮环境中LC的行为产生影响。

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