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约氏疟原虫 17XL 感染通过倾斜调节性 T 细胞和扩增 Th17 来改变树突状细胞的成熟和功能。

Plasmodium yoelii 17XL infection modified maturation and function of dendritic cells by skewing Tregs and amplificating Th17.

机构信息

Department of Basic Medical Sciences, Taizhou University Hospital, Taizhou University, No 1139 Shifu Road, Jiaojiang District, Taizhou, 318000, China.

Nursing Department, Xiang'An Hospital, Xiamen University, No 2000, Xian'an East Road, Xiang'an District, Xiamen, 361005, China.

出版信息

BMC Infect Dis. 2020 Apr 6;20(1):266. doi: 10.1186/s12879-020-04990-z.

DOI:10.1186/s12879-020-04990-z
PMID:32252652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7132900/
Abstract

BACKGROUND

Emerging data has suggested that Tregs, Th17, Th1 and Th2 are correlated with early immune mechanisms by controlling Plasmodium infection. Plasmodium infection appeared to impair the antigen presentation and maturation of DCs, leading to attenuation of specific cellular immune response ultimately. Hence, in this study, we aim to evaluate the relevance between DCs and Tregs/Th17 populations in the process and outcomes of infection with Plasmodium yoelii 17XL (P.y17XL).

METHODS

DCs detection/analysis dynamically was performed by Tregs depletion or Th17 neutralization in P.y17XL infected BALB/c mice via flow cytometry. Then the levels of cytokines production were detected using enzyme-linked mmunosorbent assay (ELISA).

RESULTS

Our results indicated that Tregs depletion or Th17 neutralization in BALB/c mice infected with P.y17XL significantly up-regulated the percentages of mDC and pDC, increased the expressions of major histocompatibility complex (MHC) class II, CD80, CD86 on DCs and the levels of IL-10/IL-12 secreted by DCs, indicating that abnormal amplification of Tregs or Th17 may damage the maturation and function of DCs during the early stage of malaria infection. Interestingly, we also found that the abnormal amplification of Th17, as well as Tregs, could inhibit the maturation of DCs.

CONCLUSIONS

Tregs skewing or Th17 amplification during the early stage of malaria infection may inhibit the maturation and function of DCs by modifying the subsets of DCs, expressions of surface molecules on DCs and secretion mode of cytokines.

摘要

背景

新出现的数据表明，Tregs、Th17、Th1 和 Th2 通过控制疟原虫感染与早期免疫机制相关。疟原虫感染似乎会损害 DC 的抗原呈递和成熟，最终导致特异性细胞免疫反应减弱。因此，在这项研究中，我们旨在评估 Plasmodium yoelii 17XL（P.y17XL）感染过程和结果中 DCs 与 Tregs/Th17 群体之间的相关性。

方法

通过流式细胞术在感染 P.y17XL 的 BALB/c 小鼠中通过 Tregs 耗竭或 Th17 中和来动态检测/分析 DCs 的检测/分析。然后使用酶联免疫吸附测定（ELISA）检测细胞因子产生水平。

结果

我们的结果表明，在感染 P.y17XL 的 BALB/c 小鼠中 Tregs 耗竭或 Th17 中和可显著上调 mDC 和 pDC 的百分比，增加 DCs 上主要组织相容性复合物（MHC）II 类、CD80、CD86 的表达以及 DCs 分泌的 IL-10/IL-12 水平，表明在疟疾感染的早期阶段，Tregs 或 Th17 的异常扩增可能会损害 DCs 的成熟和功能。有趣的是，我们还发现，Th17 的异常扩增以及 Tregs 可通过改变 DCs 的亚群、DCs 表面分子的表达和细胞因子的分泌模式来抑制 DCs 的成熟。

结论

在疟疾感染的早期阶段，Tregs 倾斜或 Th17 扩增可能通过改变 DCs 的亚群、DCs 表面分子的表达和细胞因子的分泌模式来抑制 DCs 的成熟和功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/90d8a1c96d1e/12879_2020_4990_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/709c30de6f38/12879_2020_4990_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/b444fe5382bb/12879_2020_4990_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/855b33101ca4/12879_2020_4990_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/4527a19b4b5b/12879_2020_4990_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/ac00acccb12e/12879_2020_4990_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/fcbc9d451698/12879_2020_4990_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/c6cb7e5bcbb9/12879_2020_4990_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/2b879ad97286/12879_2020_4990_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/df28973ecd3b/12879_2020_4990_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/90d8a1c96d1e/12879_2020_4990_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/709c30de6f38/12879_2020_4990_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/b444fe5382bb/12879_2020_4990_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/855b33101ca4/12879_2020_4990_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/4527a19b4b5b/12879_2020_4990_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/ac00acccb12e/12879_2020_4990_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/fcbc9d451698/12879_2020_4990_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/c6cb7e5bcbb9/12879_2020_4990_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/2b879ad97286/12879_2020_4990_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/df28973ecd3b/12879_2020_4990_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47c9/7132900/90d8a1c96d1e/12879_2020_4990_Fig10_HTML.jpg

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