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IgAV 患者 Tr1 细胞数量和功能的缺失及 IL-27 的可能作用。

Deficiency in the frequency and function of Tr1 cells in IgAV and the possible role of IL-27.

机构信息

Department of Pediatric Rheumatology and Allergy, The First Hospital of Jilin University, Changchun, China.

出版信息

Rheumatology (Oxford). 2021 Jul 1;60(7):3432-3442. doi: 10.1093/rheumatology/keaa752.

DOI:10.1093/rheumatology/keaa752
PMID:33280050
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8516516/
Abstract

OBJECTIVE

Type 1 regulatory T (Tr1) cells are involved in the pathogenesis of numerous immune-mediated diseases. However, little is known about whether and how Tr1 cells affect the development of IgA vasculitis (IgAV). We aimed to investigate this question in IgAV patients.

METHODS

. Tr1 cells in peripheral blood and kidney tissue of IgAV patients were analysed by multi-parametric flow cytometry and immunofluorescence techniques. An in vitro assay of suppression of T cell proliferation and cytokine release was performed to evaluate the function of Tr1 cells. Real-time PCR and cell stimulation in vitro were used to explore the roles of IL-27 and early growth response gene 2 (EGR2).

RESULTS

The frequency of Tr1 cells was decreased in peripheral blood but increased in kidney tissue from IgAV patients. A defective suppressive function of Tr1 cells in IgAV was observed. The frequency of Tr1 cells and the cytokines secreted by them were up-regulated in the presence of recombinant IL-27 in vitro. Moreover, IL-27 also increased the expression of EGR2. Furthermore, lower frequency of Tr1 cells during remission had a higher recurrence rate.

CONCLUSION

Tr1 cells are involved in the pathogenesis of IgAV. The low IL-27 in IgAV is responsible for impaired frequency and function of Tr1 cells, and EGR2 may be the specific transcription factor involved in the progression. Tr1 may be a risk factor for IgAV recurrence.

摘要

目的

1 型调节性 T（Tr1）细胞参与了许多免疫介导的疾病的发病机制。然而，对于 Tr1 细胞是否以及如何影响 IgA 血管炎（IgAV）的发展知之甚少。我们旨在调查 IgAV 患者中是否存在这种情况。

方法

通过多参数流式细胞术和免疫荧光技术分析 IgAV 患者外周血和肾组织中的 Tr1 细胞。进行体外抑制 T 细胞增殖和细胞因子释放的抑制试验，以评估 Tr1 细胞的功能。使用实时 PCR 和体外细胞刺激来探讨白细胞介素 27（IL-27）和早期生长反应基因 2（EGR2）的作用。

结果

IgAV 患者外周血中 Tr1 细胞的频率降低，但肾组织中 Tr1 细胞的频率增加。观察到 IgAV 中 Tr1 细胞的抑制功能缺陷。体外存在重组 IL-27 时，Tr1 细胞的频率及其分泌的细胞因子增加。此外，IL-27 还增加了 EGR2 的表达。此外，缓解期 Tr1 细胞频率较低的患者复发率更高。

结论

Tr1 细胞参与了 IgAV 的发病机制。IgAV 中较低的 IL-27 导致 Tr1 细胞频率和功能受损，EGR2 可能是参与进展的特定转录因子。Tr1 可能是 IgAV 复发的危险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/c23568a14859/keaa752f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/b160e493c00f/keaa752f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/11cb0a84831a/keaa752f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/466c6f18b3cb/keaa752f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/dfce74e7a8f4/keaa752f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/08b74e9657ca/keaa752f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/c23568a14859/keaa752f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/b160e493c00f/keaa752f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/11cb0a84831a/keaa752f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/466c6f18b3cb/keaa752f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/dfce74e7a8f4/keaa752f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/08b74e9657ca/keaa752f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69fb/8516516/c23568a14859/keaa752f6.jpg

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