Juvenile Idiopathic Arthritis

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Stephen D Anesi - One of the best experts on this subject based on the ideXlab platform.

Alberto Martini - One of the best experts on this subject based on the ideXlab platform.

  • genetic architecture distinguishes systemic Juvenile Idiopathic Arthritis from other forms of Juvenile Idiopathic Arthritis clinical and therapeutic implications
    Annals of the Rheumatic Diseases, 2017
    Co-Authors: Michael J Ombrello, Alexei A. Grom, Alberto Martini, Anne Hinks, Victoria L Arthur, Elaine F Remmers, Ioanna Tachmazidou, Dirk Foell, Marco Gattorno
    Abstract:

    Objectives Juvenile Idiopathic Arthritis (JIA) is a heterogeneous group of conditions unified by the presence of chronic childhood Arthritis without an identifiable cause. Systemic JIA (sJIA) is a rare form of JIA characterised by systemic inflammation. sJIA is distinguished from other forms of JIA by unique clinical features and treatment responses that are similar to autoinflammatory diseases. However, approximately half of children with sJIA develop destructive, long-standing Arthritis that appears similar to other forms of JIA. Using genomic approaches, we sought to gain novel insights into the pathophysiology of sJIA and its relationship with other forms of JIA. Methods We performed a genome-wide association study of 770 children with sJIA collected in nine countries by the International Childhood Arthritis Genetics Consortium. Single nucleotide polymorphisms were tested for association with sJIA. Weighted genetic risk scores were used to compare the genetic architecture of sJIA with other JIA subtypes. Results The major histocompatibility complex locus and a locus on chromosome 1 each showed association with sJIA exceeding the threshold for genome-wide significance, while 23 other novel loci were suggestive of association with sJIA. Using a combination of genetic and statistical approaches, we found no evidence of shared genetic architecture between sJIA and other common JIA subtypes. Conclusions The lack of shared genetic risk factors between sJIA and other JIA subtypes supports the hypothesis that sJIA is a unique disease process and argues for a different classification framework. Research to improve sJIA therapy should target its unique genetics and specific pathophysiological pathways.

  • systemic Juvenile Idiopathic Arthritis
    Autoimmunity Reviews, 2012
    Co-Authors: Alberto Martini
    Abstract:

    Systemic Juvenile Idiopathic Arthritis (sJIA) sets well apart from all the other forms of JIA. Several observations show that sJIA is etiopathogenically different from all the other forms of JIA and has a prominent autoinflammatory component. A major role in the pathogenesis is played by two proinflammatory cytokines, interleukin-6 and interleukin-1. The specific inhibition of these two cytokines is going to change not only the therapeutic approach to the disease but also, presumably, its long term prognosis.

  • it is time to rethink Juvenile Idiopathic Arthritis classification and nomenclature
    Annals of the Rheumatic Diseases, 2012
    Co-Authors: Alberto Martini
    Abstract:

    Juvenile Idiopathic Arthritis (JIA) is not a disease, but an exclusion diagnosis that encompasses all forms of Arthritis that begin before the age of 16 years, persist for more than 6 weeks, and are of unknown origin. This heterogeneous group of chronic arthritides has been classified on clinical and laboratory grounds to try to identify homogeneous, mutually exclusives categories suitable for etiopathogenic studies . Recent advances have shown that while some JIA categories identify quite definite disease entities, others still include heterogeneous conditions. Some aspects of JIA classification and nomenclature need therefore to be reconsidered.

  • Juvenile Idiopathic Arthritis
    BioDrugs, 2012
    Co-Authors: Angelo Ravelli, Alberto Martini
    Abstract:

    Overexpression of cytokines in inflamed joints plays an important role in joint inflammation and in damage to articular tissue. Biological agents aimed at specifically antagonising tumour necrosis factor (TNF) are effective in the treatment of adult rheumatoid Arthritis. A recent trial of etanercept, a genetically engineered fusion protein consisting of the Fc domain of human IgGl and the TNF receptor p75, has demonstrated that this agent is also well tolerated and effective in patients with Juvenile Idiopathic Arthritis (JIA). Etanercept offers a promising new alternative for patients with JIA who have persistently active Arthritis despite treatment with methotrexate. Further studies are needed to clarify whether etanercept is equally effective in the various onset types of JIA (oligoArthritis, polyArthritis and systemic Arthritis), whether it can modify disease progression and whether it can be administered safely for long periods of time to children.

  • Arthritis 3 Juvenile Idiopathic Arthritis
    The Lancet, 2011
    Co-Authors: Berent J Prakken, Salvatore Albani, Alberto Martini
    Abstract:

    Juvenile Idiopathic Arthritis is a heterogeneous group of diseases characterised by Arthritis of unknown origin with onset before age of 16 years. Pivotal studies in the past 5 years have led to substantial progress in various areas, ranging from disease classification to new treatments. Gene expression profiling studies have identified different immune mechanisms in distinct subtypes of the disease, and can help to redefine disease classification criteria. Moreover, immunological studies have shown that systemic Juvenile Idiopathic Arthritis is an acquired autoinflammatory disease, and have led to successful studies of both interleukin-1 and interleukin-6 blockade. In other forms of the disease, synovial inflammation is the consequence of a disturbed balance between proinflammatory effector cells (such as T-helper-17 cells), and anti-inflammatory regulatory cells (such as FOXP3-positive regulatory T cells). Moreover, specific soluble biomarkers (S100 proteins) can guide individual treatment. Altogether these new developments in genetics, immunology, and imaging are instrumental to better define, classify, and treat patients with Juvenile Idiopathic Arthritis.

Hakon Hakonarson - One of the best experts on this subject based on the ideXlab platform.

  • genetic architecture study of rheumatoid Arthritis and Juvenile Idiopathic Arthritis
    PeerJ, 2020
    Co-Authors: Jun Jia, Xueming Yao, Yuhang Zhang, Xiaohao Yang, Ping Wang, Qianghua Xia, Hakon Hakonarson
    Abstract:

    Background Rheumatoid Arthritis and Juvenile Idiopathic Arthritis are two types of autoimmune diseases with inflammation at the joints, occurring to adults and children respectively. There are phenotypic overlaps between these two types of diseases, despite the age difference in patient groups. Methods To systematically compare the genetic architecture of them, we conducted analyses at gene and pathway levels and constructed protein-protein-interaction network based on summary statistics of genome-wide association studies of these two diseases. We examined their difference and similarity at each level. Results We observed extensive overlap in significant SNPs and genes at the human leukocyte antigen region. In addition, several SNPs in other regions of the human genome were also significantly associated with both diseases. We found significantly associated genes enriched in 32 pathways shared by both diseases. Excluding genes in the human leukocyte antigen region, significant enrichment is present for pathways like interleukin-27 pathway and NO2-dependent interleukin-12 pathway in natural killer cells. Discussion The identification of commonly associated genes and pathways may help in finding population at risk for both diseases, as well as shed light on repositioning and designing drugs for both diseases.

Peter Y Chang - One of the best experts on this subject based on the ideXlab platform.

Arash Maleki - One of the best experts on this subject based on the ideXlab platform.

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