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人类Vogt-小柳-原田病的外周免疫格局及自然杀伤样B细胞

Peripheral immune landscape and natural killer-like B cells in human Vogt-Koyanagi-Harada disease.

作者信息

Li He, Zhu Lei, Liu Xiuxing, Xie Lihui, Wang Rong, Li Zhaohuai, Huang Zhaohao, Yang Shizhao, Chen Binyao, Ye Jinguo, Zheng Yingfeng, Su Wenru

机构信息

State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou 510060, China.

出版信息

Life Med. 2022 Dec 8;1(3):387-400. doi: 10.1093/lifemedi/lnac047. eCollection 2022 Dec.

DOI:10.1093/lifemedi/lnac047
PMID:39872747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11749541/
Abstract

Vogt-Koyanagi-Harada (VKH) disease is a systemic autoimmune disorder threatening the eyesight. The pathogenic mechanisms and biomarkers reflecting disease severity and predicting treatment response require further exploration. Here, we performed a single-cell analysis of peripheral blood mononuclear cells (PBMC) obtained from eight patients with VKH disease and eight healthy controls to comprehensively delineate the changes in VKH disease. We showed a mixture of inflammation, effector, and exhausted states for PBMCs in VKH disease. Notably, our study implicated a newly identified B cell subset, natural killer-like B cells (K-BC) characterized by expressing CD19 and CD56, was correlated with VKH disease. K-BCs expanded in VKH disease, fell back after effective treatment, and promoted the differentiation of pathogenic T cells. Overall, we mapped the peripheral immune cell atlas in VKH disease and indicated the pathogenic role and potential value in predicting treatment response of K-BCs.

摘要

伏格特-小柳-原田(VKH)病是一种威胁视力的全身性自身免疫性疾病。其致病机制以及反映疾病严重程度和预测治疗反应的生物标志物仍需进一步探索。在此,我们对8例VKH病患者和8例健康对照者的外周血单个核细胞(PBMC)进行了单细胞分析,以全面描绘VKH病中的变化。我们发现VKH病患者的PBMC呈现出炎症、效应和耗竭状态的混合。值得注意的是,我们的研究表明一种新鉴定的B细胞亚群,即表达CD19和CD56的自然杀伤样B细胞(K-BC)与VKH病相关。K-BC在VKH病中扩增,有效治疗后回落,并促进致病性T细胞的分化。总体而言,我们绘制了VKH病的外周免疫细胞图谱,并指出了K-BC在预测治疗反应中的致病作用和潜在价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/23e138f9ec71/lnac047_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/357faee232fa/lnac047_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/6a3973a07253/lnac047_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/3b42536351c1/lnac047_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/44fdcb1b7119/lnac047_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/921c373a28af/lnac047_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/a7dc989abd3d/lnac047_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/23e138f9ec71/lnac047_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/357faee232fa/lnac047_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/6a3973a07253/lnac047_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/3b42536351c1/lnac047_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/44fdcb1b7119/lnac047_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/921c373a28af/lnac047_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/a7dc989abd3d/lnac047_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b3d/11749541/23e138f9ec71/lnac047_fig6.jpg

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Int Immunopharmacol. 2021 Nov;100:108161. doi: 10.1016/j.intimp.2021.108161. Epub 2021 Sep 20.
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Deficiency of IL-27 Signaling Exacerbates Experimental Autoimmune Uveitis with Elevated Uveitogenic Th1 and Th17 Responses.
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Nat Rev Gastroenterol Hepatol. 2021 Jul;18(7):451-452. doi: 10.1038/s41575-021-00471-z.
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Natural Killer-Like B Cells Secreting Interleukin-18 Induces a Proinflammatory Response in Periodontitis.自然杀伤样 B 细胞分泌白细胞介素-18 可诱导牙周炎的促炎反应。
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