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.
Highlights
Juvenile idiopathic arthritis (JIA) is a common type of chronic rheumatic diseases affecting children with the age of onset under 16 years, and an important cause of disability
These findings suggested that the inflammatory injuries in JIA and rheumatoid arthritis (RA) could be caused by abnormal methylation, and levels of methylation are related to the types and stages of disease [124]
Though JIA was classified into seven subtypes, phenotypic overlap was observed between subtypes, suggesting shared genetic/epigenetic basis
Summary
Juvenile idiopathic arthritis (JIA) is a common type of chronic rheumatic diseases affecting children with the age of onset under 16 years, and an important cause of disability. Epidemiological studies showed that incidence rate of JIA ranges from 1.6 to 23 per 100,000 children annually and the prevalence of JIA was about 3.8–400 per 100,000 children in Europe [1]. Its negative effects on children’s physical development, as well as psychiatric development, cause serious damage to the quality of life of affected children, causing pain of active joints, physical disability, anxiety, and depression. JIA needs aggressive treatment to control its symptoms. For this difficult disease, it is important to understand the underlying molecular mechanisms of the development of JIA systematically through unbiased approaches. People have started to gain knowledge about the multiomics architecture of JIA, thanks to the advance of high-throughput omics technologies, which is the focus of this review article
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