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The Multi-Omics Architecture of Juvenile Idiopathic Arthritis

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 mino...

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Autores principales: Hou, Xiaoyuan, Qu, Huiqi, Zhang, Sipeng, Qi, Xiaohui, Hakonarson, Hakon, Xia, Qianghua, Li, Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7602566/
https://www.ncbi.nlm.nih.gov/pubmed/33076506
http://dx.doi.org/10.3390/cells9102301
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author Hou, Xiaoyuan
Qu, Huiqi
Zhang, Sipeng
Qi, Xiaohui
Hakonarson, Hakon
Xia, Qianghua
Li, Jin
author_facet Hou, Xiaoyuan
Qu, Huiqi
Zhang, Sipeng
Qi, Xiaohui
Hakonarson, Hakon
Xia, Qianghua
Li, Jin
author_sort Hou, Xiaoyuan
collection PubMed
description 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.
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spelling pubmed-76025662020-11-01 The Multi-Omics Architecture of Juvenile Idiopathic Arthritis Hou, Xiaoyuan Qu, Huiqi Zhang, Sipeng Qi, Xiaohui Hakonarson, Hakon Xia, Qianghua Li, Jin Cells Review 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. MDPI 2020-10-15 /pmc/articles/PMC7602566/ /pubmed/33076506 http://dx.doi.org/10.3390/cells9102301 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Hou, Xiaoyuan
Qu, Huiqi
Zhang, Sipeng
Qi, Xiaohui
Hakonarson, Hakon
Xia, Qianghua
Li, Jin
The Multi-Omics Architecture of Juvenile Idiopathic Arthritis
title The Multi-Omics Architecture of Juvenile Idiopathic Arthritis
title_full The Multi-Omics Architecture of Juvenile Idiopathic Arthritis
title_fullStr The Multi-Omics Architecture of Juvenile Idiopathic Arthritis
title_full_unstemmed The Multi-Omics Architecture of Juvenile Idiopathic Arthritis
title_short The Multi-Omics Architecture of Juvenile Idiopathic Arthritis
title_sort multi-omics architecture of juvenile idiopathic arthritis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7602566/
https://www.ncbi.nlm.nih.gov/pubmed/33076506
http://dx.doi.org/10.3390/cells9102301
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