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Mediators of Inflammation
Volume 2017, Article ID 2405291, 13 pages
Research Article

Cytokine Imbalance as a Common Mechanism in Both Psoriasis and Rheumatoid Arthritis

1Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China
2Institute of Clinical Pharmacology, Beijing An Zhen Hospital, Capital Medical University, Beijing 100029, China
3Department of Dermatology, China-Japan Friendship Hospital, Beijing 100029, China
4Department of Dermatology, Beijing Hospital of Traditional Chinese Medicine, Beijing 100010, China
5Department of Dermatology and Venerology, Peking University First Hospital, Beijing 100034, China
6Department of Dermatology and Skin Science, University of British Columbia, Vancouver, BC, Canada
7Molecular Medicine Laboratory and Chieng Genomics Center, Vancouver Coastal Health Research Institute, Vancouver, BC, Canada
8Institute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong
9E-Institute of Chinese Traditional Internal Medicine, Shanghai Municipal Education Commission, Shanghai 201203, China
10Institute of Clinical Medicine, China-Japan Friendship Hospital, Beijing 100029, China

Correspondence should be addressed to Youwen Zhou; ac.cbu@uohz.newuoy, Aiping Lu; kh.ude.ubkh@ulgnipia, and Cheng Xiao; moc.621@2182002cx

Received 11 October 2016; Accepted 30 November 2016; Published 25 January 2017

Academic Editor: Qingdong Guan

Copyright © 2017 Yong Tan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Psoriasis (PS) and rheumatoid arthritis (RA) are immune-mediated inflammatory diseases. Previous studies showed that these two diseases had a common pathogenesis, but the precise molecular mechanism remains unclear. In this study, RNA sequencing of peripheral blood mononuclear cells was employed to explore both the differentially expressed genes (DEGs) of 10 PS and 10 RA patients compared with those of 10 healthy volunteers and the shared DEGs between these two diseases. Bioinformatics network analysis was used to reveal the connections among the shared DEGs and the corresponding molecular mechanism. In total, 120 and 212 DEGs were identified in PS and RA, respectively, and 31 shared DEGs were identified. Bioinformatics analysis indicated that the cytokine imbalance relevant to key molecules (such as extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), tumor necrosis factor (TNF), colony-stimulating factor 3 (CSF3), interleukin- (IL-) 6, and interferon gene (IFNG)) and canonical signaling pathways (such as the complement system, antigen presentation, macropinocytosis signaling, nuclear factor-kappa B (NF-κB) signaling, and IL-17 signaling) was responsible for the common comprehensive mechanism of PS and RA. Our findings provide a better understanding of the pathogenesis of PS and RA, suggesting potential strategies for treating and preventing both diseases. This study may also provide a new paradigm for illuminating the common pathogenesis of different diseases.