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视神经脊髓炎谱系疾病患者 Tr1 细胞上 CD226 的表达上调。

Expression of CD226 is upregulated on Tr1 cells from neuromyelitis optica spectrum disorder patients.

机构信息

Department of Neurology, Xianyang Hospital of Yan'an University, Xianyang, China.

Department of Immunology, Medical College of Yan'an University, Yan'an, China.

出版信息

Brain Behav. 2022 Jun;12(6):e2623. doi: 10.1002/brb3.2623. Epub 2022 May 19.

DOI:10.1002/brb3.2623
PMID:35587519
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9226801/
Abstract

BACKGROUND

Neuromyelitis optica spectrum disorder (NMOSD) is a central and acute demyelinating disease of the central nervous system with unusual clinical course. The development of novel biomarkers for NMOSD is critical for implementing effective clinical treatment. CD226 is known to be expressed on many types of peripheral lymphoid cells. However, the expression level and function of CD226 on type 1 T regulatory (Tr1) cells during NMOSD is unknown.

METHODS

Eighteen patients with NMOSD and 10 healthy volunteers were enrolled in the test group to probe the difference of CD226 expression on Tr1 cells using flow cytometric analysis.

RESULTS

The expression of CD226 on Tr1 cells exhibited significantly increased tendency in NMOSD patients. Additionally, methylprednisolone and rituximab treatment decreased the expression of CD226 on Tr1 cells. Furthermore, the expression of CD226 on Tr1 cells was correlated with disease severity.

CONCLUSION

This study provides a new basic insight into CD226 expression pattern on Tr1 cells, which have great potential to be biomarkers for monitoring the development and treatment of NMOSD.

摘要

背景

视神经脊髓炎谱系疾病（NMOSD）是一种中枢和急性脱髓鞘疾病，具有不同寻常的临床病程。开发 NMOSD 的新型生物标志物对于实施有效的临床治疗至关重要。CD226 已知在许多类型的外周淋巴样细胞上表达。然而，在 NMOSD 期间，CD226 在 1 型 T 调节（Tr1）细胞上的表达水平和功能尚不清楚。

方法

将 18 名 NMOSD 患者和 10 名健康志愿者纳入实验组，使用流式细胞术分析探测 Tr1 细胞上 CD226 表达的差异。

结果

NMOSD 患者 Tr1 细胞上 CD226 的表达呈显著增加趋势。此外，甲基强的松龙和利妥昔单抗治疗降低了 Tr1 细胞上 CD226 的表达。此外，Tr1 细胞上 CD226 的表达与疾病严重程度相关。

结论

本研究为 Tr1 细胞上 CD226 表达模式提供了新的基础见解，这对于监测 NMOSD 的发展和治疗具有很大的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/3fc4c0ab007f/BRB3-12-e2623-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/a57b54db7fa6/BRB3-12-e2623-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/334d609d240e/BRB3-12-e2623-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/a9b0c870a2ce/BRB3-12-e2623-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/f25ece84b3dd/BRB3-12-e2623-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/769de7c4677d/BRB3-12-e2623-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/3fc4c0ab007f/BRB3-12-e2623-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/a57b54db7fa6/BRB3-12-e2623-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/334d609d240e/BRB3-12-e2623-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/a9b0c870a2ce/BRB3-12-e2623-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/f25ece84b3dd/BRB3-12-e2623-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/769de7c4677d/BRB3-12-e2623-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/9226801/3fc4c0ab007f/BRB3-12-e2623-g007.jpg

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CD226 deficiency on regulatory T cells aggravates renal fibrosis via up-regulation of Th2 cytokines through miR-340.
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