IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma

Lung adenocarcinoma is one of the leading causes of cancer-related death worldwide. Low expression of Interleukin-33 (IL-33) was reported to be associated with the progression of pulmonary adenocarcinoma. However, the IL-33-mediated immunoregulation in pulmonary adenocarcinoma remains unclear. In th...

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Main Authors: Jiguang Zhang, Yangming Chen, Kai Chen, Yunchao Huang, Xunyu Xu, Qianshun Chen, Chen Huang, Jiewei Luo, Xing Lin
Format: Article
Language:English
Published: Taylor & Francis Group 2019-12-01
Series:Artificial Cells, Nanomedicine, and Biotechnology
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/21691401.2019.1596926
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author Jiguang Zhang
Yangming Chen
Kai Chen
Yunchao Huang
Xunyu Xu
Qianshun Chen
Chen Huang
Jiewei Luo
Xing Lin
author_facet Jiguang Zhang
Yangming Chen
Kai Chen
Yunchao Huang
Xunyu Xu
Qianshun Chen
Chen Huang
Jiewei Luo
Xing Lin
author_sort Jiguang Zhang
collection DOAJ
description Lung adenocarcinoma is one of the leading causes of cancer-related death worldwide. Low expression of Interleukin-33 (IL-33) was reported to be associated with the progression of pulmonary adenocarcinoma. However, the IL-33-mediated immunoregulation in pulmonary adenocarcinoma remains unclear. In this study, we found that IL-33 treatment evidently repressed tumour growth, induced CD4+ T cells infiltration and IL-17 expression in pulmonary adenocarcinoma. Notably, IL-33 treatment increased the number of Dendritic Cells (DCs) in pulmonary adenocarcinoma. More importantly, IL-33 induced maturation and regulated the function of DCs by increasing expression of DCs mature markers (CD40 and CD80, CD86) DCs-function-related gene including antigen presentation genes (HLA-DMA, HLA-DMB and CD74) and cytokines (IL-1β, IL-6 and TNF). Mechanistic studies demonstrated that IL-33 treatment induced DCs maturation by upregulating CYLD expression in DCs. In addition, CYLD played an important role in DCs-induced T cell proliferation and IL-17 secretion. In conclusion, our study demonstrated that IL-33 mediated immunoregulation in pulmonary adenocarcinoma by improving DC-induced T cell proliferation by upregulating CYLD expression.
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spelling doaj.art-41268b5f24f44f219aa93812116ce5152022-12-22T01:10:38ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2019-12-014711335134110.1080/21691401.2019.1596926IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinomaJiguang Zhang0Yangming Chen1Kai Chen2Yunchao Huang3Xunyu Xu4Qianshun Chen5Chen Huang6Jiewei Luo7Xing Lin8Department of Thoracic Surgery, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, Fujian, ChinaDepartment of Thoracic Surgery, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, Fujian, ChinaDepartment of Thoracic Surgery, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, Fujian, ChinaDepartment of thoracic surgery, Yunnan Cancer Hospital, the Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, ChinaDepartment of Thoracic Surgery, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, Fujian, ChinaDepartment of Thoracic Surgery, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, Fujian, ChinaDepartment of Thoracic Surgery, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, Fujian, ChinaDepartment of traditional Chinese medicine, Fujian Province Hospital, School of clinical medicine, Fujian Medical University, Fuzhou, Fujian, ChinaDepartment of Thoracic Surgery, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, Fujian, ChinaLung adenocarcinoma is one of the leading causes of cancer-related death worldwide. Low expression of Interleukin-33 (IL-33) was reported to be associated with the progression of pulmonary adenocarcinoma. However, the IL-33-mediated immunoregulation in pulmonary adenocarcinoma remains unclear. In this study, we found that IL-33 treatment evidently repressed tumour growth, induced CD4+ T cells infiltration and IL-17 expression in pulmonary adenocarcinoma. Notably, IL-33 treatment increased the number of Dendritic Cells (DCs) in pulmonary adenocarcinoma. More importantly, IL-33 induced maturation and regulated the function of DCs by increasing expression of DCs mature markers (CD40 and CD80, CD86) DCs-function-related gene including antigen presentation genes (HLA-DMA, HLA-DMB and CD74) and cytokines (IL-1β, IL-6 and TNF). Mechanistic studies demonstrated that IL-33 treatment induced DCs maturation by upregulating CYLD expression in DCs. In addition, CYLD played an important role in DCs-induced T cell proliferation and IL-17 secretion. In conclusion, our study demonstrated that IL-33 mediated immunoregulation in pulmonary adenocarcinoma by improving DC-induced T cell proliferation by upregulating CYLD expression.https://www.tandfonline.com/doi/10.1080/21691401.2019.1596926Interleukin 33pulmonary adenocarcinomaDCsCYLDCD4+ T cellsIL-17
spellingShingle Jiguang Zhang
Yangming Chen
Kai Chen
Yunchao Huang
Xunyu Xu
Qianshun Chen
Chen Huang
Jiewei Luo
Xing Lin
IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma
Artificial Cells, Nanomedicine, and Biotechnology
Interleukin 33
pulmonary adenocarcinoma
DCs
CYLD
CD4+ T cells
IL-17
title IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma
title_full IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma
title_fullStr IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma
title_full_unstemmed IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma
title_short IL-33 drives the antitumour effects of dendritic cells via upregulating CYLD expression in pulmonary adenocarcinoma
title_sort il 33 drives the antitumour effects of dendritic cells via upregulating cyld expression in pulmonary adenocarcinoma
topic Interleukin 33
pulmonary adenocarcinoma
DCs
CYLD
CD4+ T cells
IL-17
url https://www.tandfonline.com/doi/10.1080/21691401.2019.1596926
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