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Review
. 2020 Oct 15;9(10):2301.
doi: 10.3390/cells9102301.

The Multi-Omics Architecture of Juvenile Idiopathic Arthritis

Affiliations
Review

The Multi-Omics Architecture of Juvenile Idiopathic Arthritis

Xiaoyuan Hou et al. Cells. .

Abstract

Juvenile idiopathic arthritis (JIA) is highly heterogeneous in terms of etiology and clinical presentation with ambiguity in JIA classification. The advance of high-throughput omics technologies in recent years has gained us significant knowledge about the molecular mechanisms of JIA. Besides a minor proportion of JIA cases as monogenic, most JIA cases are polygenic disease caused by autoimmune mechanisms. A number of HLA alleles (including both HLA class I and class II genes), and 23 non-HLA genetic loci have been identified of association with different JIA subtypes. Omics technologies, i.e., transcriptome profiling and epigenomic analysis, contributed significant knowledge on the molecular mechanisms of JIA in addition to the genetic approach. New molecular knowledge on different JIA subtypes enables us to reconsider the JIA classification, but also highlights novel therapeutic targets to develop a cure for the devastating JIA.

Keywords: epigenetics; genetics; genome-wide association study; juvenile idiopathic arthritis; transcriptome.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Pathway analysis of 33 genes at the JIA GWAS loci. The enrichment ratio for the functional categories in the KEGG database is shown on the X-axis and the log of the FDR is shown on the Y-axis, indicating the degree by which the significant categories stand out from the background. The size and color of the dot are proportional to the number of input genes falling into each pathway.
Figure 2
Figure 2
Protein–protein interaction (PPI) analysis of the 33 genes in the GWAS loci. Each node represents each gene product at the JIA GWAS loci and edges between nodes represent protein–protein interactions.

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