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白塞病中抗原呈递细胞产生的白细胞介素-12家族细胞因子引发的辅助性T细胞反应失衡及遗传背景

Skewed Helper T-Cell Responses to IL-12 Family Cytokines Produced by Antigen-Presenting Cells and the Genetic Background in Behcet's Disease.

作者信息

Shimizu Jun, Kaneko Fumio, Suzuki Noboru

机构信息

Department of Immunology and Medicine, St. Marianna University School of Medicine, Sugao 2-16-1, Miyamae-ku, Kawasaki 216-8511, Japan.

Department of Dermatology, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan.

出版信息

Genet Res Int. 2013;2013:363859. doi: 10.1155/2013/363859. Epub 2013 Dec 30.

DOI:10.1155/2013/363859
PMID:24490076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3892938/
Abstract

Behcet's disease (BD) is a multisystemic inflammatory disease and is characterized by recurrent attacks on eyes, brain, skin, and gut. There is evidence that skewed T-cell responses contributed to its pathophysiology in patients with BD. Recently, we found that Th17 cells, a new helper T (Th) cell subset, were increased in patients with BD, and both Th type 1 (Th1) and Th17 cell differentiation signaling pathways were overactivated. Several researches revealed that genetic polymorphisms in Th1/Th17 cell differentiation signaling pathways were associated with the onset of BD. Here, we summarize current findings on the Th cell subsets, their contribution to the pathogenesis of BD and the genetic backgrounds, especially in view of IL-12 family cytokine production and pattern recognition receptors of macrophages/monocytes.

摘要

白塞病(BD)是一种多系统炎症性疾病,其特征是眼睛、大脑、皮肤和肠道反复发病。有证据表明,T细胞反应失衡在BD患者的病理生理学中起作用。最近,我们发现,一种新的辅助性T(Th)细胞亚群——Th17细胞,在BD患者中增多,并且Th1型(Th1)和Th17细胞分化信号通路均过度激活。多项研究表明,Th1/Th17细胞分化信号通路中的基因多态性与BD的发病有关。在此,我们总结了目前关于Th细胞亚群的研究结果、它们在BD发病机制中的作用以及遗传背景,特别是从白细胞介素-12家族细胞因子的产生和巨噬细胞/单核细胞的模式识别受体的角度进行总结。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e8/3892938/45fd2e49c899/GRI2013-363859.006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e8/3892938/8ff924d448f9/GRI2013-363859.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e8/3892938/90204fd01857/GRI2013-363859.002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e8/3892938/f0d3cab0ce95/GRI2013-363859.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e8/3892938/45fd2e49c899/GRI2013-363859.006.jpg

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