Suppr超能文献

在腔隙性病变中,CD163+CD11c+树突状细胞的密度增加,而 CD103+树突状细胞的密度减少。

Density of CD163+ CD11c+ dendritic cells increases and CD103+ dendritic cells decreases in the coeliac lesion.

机构信息

Centre for Immune Regulation, Institute of Immunology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.

出版信息

Scand J Immunol. 2011 Aug;74(2):186-94. doi: 10.1111/j.1365-3083.2011.02549.x.

Abstract

Coeliac disease is a chronic inflammation of the intestinal mucosa controlled by gluten-specific T cells restricted by disease-associated HLA-DQ molecules. We have previously reported that mucosal CD11c(+) dendritic cells (DCs) are responsible for activation of gluten-reactive T cells within the coeliac lesion. In mice, intestinal CD11c(+) DCs comprise several functionally distinct subsets. Here, we report that HLA-DQ(+) antigen-presenting cells (APCs) in normal human duodenal mucosa can be divided into four subsets with striking similarities to those described in mice: CD163(+) CD11c(-) macrophages (74%), and CD11c(+) cells expressing either CD163 (7%), CD103 (11%) or CD1c (13%). CD103(+) and CD1c(+) DCs belonged to partly overlapping populations, whereas CD163(+) CD11c(+) APCs appeared to be a distinct population. In the coeliac lesion, we found increased density of CD163(+) CD11c(+) APCs, whereas the density of CD103(+) and CD1c(+) DCs was decreased, suggesting that distinct subpopulations of APCs in coeliac disease may exert different functions in the pathogenesis.

摘要

自身免疫性疾病

自身免疫性疾病是一种由 gluten-specific T 细胞控制的慢性肠黏膜炎症,这些细胞受到疾病相关的 HLA-DQ 分子的限制。我们之前曾报道过,黏膜 CD11c(+)树突状细胞(DCs)是在乳糜泻病变中激活 gluten-reactive T 细胞的原因。在小鼠中,肠道 CD11c(+)DCs 包括几个功能不同的亚群。在这里,我们报告正常人类十二指肠黏膜中的 HLA-DQ(+)抗原呈递细胞(APCs)可以分为四个亚群,与在小鼠中描述的亚群具有惊人的相似性:CD163(+) CD11c(-)巨噬细胞(74%),以及表达 CD163(7%)、CD103(11%)或 CD1c(13%)的 CD11c(+)细胞。CD103(+)和 CD1c(+)DC 属于部分重叠的群体,而 CD163(+) CD11c(+)APCs 似乎是一个独特的群体。在乳糜泻病变中,我们发现 CD163(+) CD11c(+)APCs 的密度增加,而 CD103(+)和 CD1c(+)DC 的密度降低,这表明乳糜泻疾病中不同的 APC 亚群可能在发病机制中发挥不同的作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验