Genetic Background and Molecular Mechanisms of Juvenile Idiopathic Arthritis

Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatic disease in the paediatric population. JIA comprises a heterogeneous group of disorders with different onset patterns and clinical presentations with the only element in common being chronic joint inflammation. This review sough...

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Main Authors: Saverio La Bella, Marta Rinaldi, Armando Di Ludovico, Giulia Di Donato, Giulio Di Donato, Vincenzo Salpietro, Francesco Chiarelli, Luciana Breda
Format: Article
Language:English
Published: MDPI AG 2023-01-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/24/3/1846
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author Saverio La Bella
Marta Rinaldi
Armando Di Ludovico
Giulia Di Donato
Giulio Di Donato
Vincenzo Salpietro
Francesco Chiarelli
Luciana Breda
author_facet Saverio La Bella
Marta Rinaldi
Armando Di Ludovico
Giulia Di Donato
Giulio Di Donato
Vincenzo Salpietro
Francesco Chiarelli
Luciana Breda
author_sort Saverio La Bella
collection DOAJ
description Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatic disease in the paediatric population. JIA comprises a heterogeneous group of disorders with different onset patterns and clinical presentations with the only element in common being chronic joint inflammation. This review sought to evaluate the most relevant and up-to-date evidence on current knowledge regarding the pathogenesis of JIA subtypes to provide a better understanding of these disorders. Despite significant improvements over the past decade, the aetiology and molecular mechanisms of JIA remain unclear. It has been suggested that the immunopathogenesis is characterised by complex interactions between genetic background and environmental factors that may differ between JIA subtypes. Human leukocyte antigen (HLA) haplotypes and non-HLA genes play a crucial role in the abnormal activation of both innate and adaptive immune cells that cooperate in causing the inflammatory process. This results in the involvement of proinflammatory cytokines, including tumour necrosis factor (TNF)α, interleukin (IL)-1, IL-6, IL-10, IL-17, IL-21, IL-23, and others. These mediators, interacting with the surrounding tissue, cause cartilage stress and bone damage, including irreversible erosions. The purpose of this review is to provide a comprehensive overview of the genetic background and molecular mechanisms of JIA.
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spelling doaj.art-8dd0bbaee12c49708edcfa1d16020b432023-11-16T16:48:35ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-01-01243184610.3390/ijms24031846Genetic Background and Molecular Mechanisms of Juvenile Idiopathic ArthritisSaverio La Bella0Marta Rinaldi1Armando Di Ludovico2Giulia Di Donato3Giulio Di Donato4Vincenzo Salpietro5Francesco Chiarelli6Luciana Breda7Paediatric Department, University of Chieti “G. D’Annunzio”, 66100 Chieti, ItalyPaediatric Department, Buckinghamshire Healthcare NHS Trust, Aylesbury-Thames Valley Deanery, Aylesbury HP21 8AL, UKPaediatric Department, University of Chieti “G. D’Annunzio”, 66100 Chieti, ItalyPaediatric Department, University of Chieti “G. D’Annunzio”, 66100 Chieti, ItalyPaediatric Department, University of L’Aquila, 67100 L’Aquila, ItalyPaediatric Department, University of L’Aquila, 67100 L’Aquila, ItalyPaediatric Department, University of Chieti “G. D’Annunzio”, 66100 Chieti, ItalyPaediatric Department, University of Chieti “G. D’Annunzio”, 66100 Chieti, ItalyJuvenile idiopathic arthritis (JIA) is the most common chronic rheumatic disease in the paediatric population. JIA comprises a heterogeneous group of disorders with different onset patterns and clinical presentations with the only element in common being chronic joint inflammation. This review sought to evaluate the most relevant and up-to-date evidence on current knowledge regarding the pathogenesis of JIA subtypes to provide a better understanding of these disorders. Despite significant improvements over the past decade, the aetiology and molecular mechanisms of JIA remain unclear. It has been suggested that the immunopathogenesis is characterised by complex interactions between genetic background and environmental factors that may differ between JIA subtypes. Human leukocyte antigen (HLA) haplotypes and non-HLA genes play a crucial role in the abnormal activation of both innate and adaptive immune cells that cooperate in causing the inflammatory process. This results in the involvement of proinflammatory cytokines, including tumour necrosis factor (TNF)α, interleukin (IL)-1, IL-6, IL-10, IL-17, IL-21, IL-23, and others. These mediators, interacting with the surrounding tissue, cause cartilage stress and bone damage, including irreversible erosions. The purpose of this review is to provide a comprehensive overview of the genetic background and molecular mechanisms of JIA.https://www.mdpi.com/1422-0067/24/3/1846juvenile idiopathic arthritisJIAmolecular mechanismspaediatric rheumatology
spellingShingle Saverio La Bella
Marta Rinaldi
Armando Di Ludovico
Giulia Di Donato
Giulio Di Donato
Vincenzo Salpietro
Francesco Chiarelli
Luciana Breda
Genetic Background and Molecular Mechanisms of Juvenile Idiopathic Arthritis
International Journal of Molecular Sciences
juvenile idiopathic arthritis
JIA
molecular mechanisms
paediatric rheumatology
title Genetic Background and Molecular Mechanisms of Juvenile Idiopathic Arthritis
title_full Genetic Background and Molecular Mechanisms of Juvenile Idiopathic Arthritis
title_fullStr Genetic Background and Molecular Mechanisms of Juvenile Idiopathic Arthritis
title_full_unstemmed Genetic Background and Molecular Mechanisms of Juvenile Idiopathic Arthritis
title_short Genetic Background and Molecular Mechanisms of Juvenile Idiopathic Arthritis
title_sort genetic background and molecular mechanisms of juvenile idiopathic arthritis
topic juvenile idiopathic arthritis
JIA
molecular mechanisms
paediatric rheumatology
url https://www.mdpi.com/1422-0067/24/3/1846
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