Both HLA class II and class III DNA polymorphisms are linked to juvenile rheumatoid arthritis susceptibility

Vicário, José L.; Martı́nez-Laso, Jorge; Gómez-Reino, Juan J.; Gomez-Reino, Francisco J.; Regueiro, José R.; Corell, Alfredo; Segurado, Oscar G.; Arnaiz‐Villena, Antonio

doi:10.1016/0090-1229(90)90165-m

Cited by 23 publications

(5 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Patients with complement deficiencies or functional asplenia, such as some SLE122 and polyarticular JIA123 124 patients, are at increased risk of acquiring Hib, meningococcal and pneumococcal infections 122. Vaccinations against these pathogens are recommended when pathogen-specific antibody concentrations are insufficient.…”

Section: Resultsmentioning

confidence: 99%

EULAR recommendations for vaccination in paediatric patients with rheumatic diseases

Heijstek

Bruin

Bijl

et al. 2011

Annals of the Rheumatic Diseases

197

177

View full text Add to dashboard Cite

Evidence-based recommendations for vaccination of paediatric patients with rheumatic diseases (PaedRD) were developed by following the EULAR standardised procedures for guideline development. The EULAR task force consisted of (paediatric) rheumatologists/immunologists, one expert in vaccine evaluation, one expert in public health and infectious disease control, and one epidemiologist. A systematic literature review was conducted in MEDLINE, EMBASE, and abstracts of the EULAR and American College of Rheumatology meetings of 2008/9. The level of evidence and strength of recommendation were based on customary scoring systems. Delphi voting was applied to assess the level of agreement between task force members. 107 papers and eight abstracts were used. The majority of papers considered seasonal influenza (41) or pneumococcal (23) vaccination. 26 studies were performed specifically in paediatric patients, and the majority in adult rheumatoid arthritis and systemic lupus erythematosus patients. Fifteen recommendations were developed with an overall agreement of 91.7%. More research is needed on the safety and immunogenicity of (live-attenuated) vaccination in PaedRD, particularly in those using biologicals, and the effect of vaccination on prevention of infections.

show abstract

Section: Resultsmentioning

confidence: 99%

EULAR recommendations for vaccination in paediatric patients with rheumatic diseases

Heijstek

Bruin

Bijl

et al. 2011

Annals of the Rheumatic Diseases

197

177

View full text Add to dashboard Cite

show abstract

“…Additionally, evidence from the literature suggests that maternal smoking during pregnancy can also be a risk factor for JIA ( 44 , 50 ). Genetic predisposition to JIA is mainly due to human leukocyte antigen (HLA) class II molecules, although HLA class I molecules and non-HLA genes have also been implicated, depending on the disease category ( 24 , 25 , 29 , 51 – 57 ).…”

Section: Etiology and Risk Factors Of Juvenile Idiopathic Arthritismentioning

confidence: 99%

B Cells on the Stage of Inflammation in Juvenile Idiopathic Arthritis: Leading or Supporting Actors in Disease Pathogenesis?

Moura

Fonseca

2022

Front. Med.

View full text Add to dashboard Cite

Juvenile idiopathic arthritis (JIA) is a term that collectively refers to a group of chronic childhood arthritides, which together constitute the most common rheumatic condition in children. The International League of Associations for Rheumatology (ILAR) criteria define seven categories of JIA: oligoarticular, polyarticular rheumatoid factor (RF) negative (RF-), polyarticular RF positive (RF+), systemic, enthesitis-related arthritis, psoriatic arthritis, and undifferentiated arthritis. The ILAR classification includes persistent and extended oligoarthritis as subcategories of oligoarticular JIA, but not as distinct categories. JIA is characterized by a chronic inflammatory process affecting the synovia that begins before the age of 16 and persists at least 6 weeks. If not treated, JIA can cause significant disability and loss of quality of life. Treatment of JIA is adjusted according to the severity of the disease as combinations of non-steroidal anti-inflammatory drugs (NSAIDs), synthetic and/ or biological disease modifying anti-rheumatic drugs (DMARDs). Although the disease etiology is unknown, disturbances in innate and adaptive immune responses have been implicated in JIA development. B cells may have important roles in JIA pathogenesis through autoantibody production, antigen presentation, cytokine release and/ or T cell activation. The study of B cells has not been extensively explored in JIA, but evidence from the literature suggests that B cells might have indeed a relevant role in JIA pathophysiology. The detection of autoantibodies such as antinuclear antibodies (ANA), RF and anti-citrullinated protein antibodies (ACPA) in JIA patients supports a breakdown in B cell tolerance. Furthermore, alterations in B cell subpopulations have been documented in peripheral blood and synovial fluid from JIA patients. In fact, altered B cell homeostasis, B cell differentiation and B cell hyperactivity have been described in JIA. Of note, B cell depletion therapy with rituximab has been shown to be an effective and well-tolerated treatment in children with JIA, which further supports B cell intervention in disease development.

show abstract

“…In the past few decades, studies have provided multiple lines of evidence that polyarthritis RF-negative subtype has a strong association with HLA Class II alleles DRB1*08 and DPB1*03 , and HLA Class I allele A2 [ 45 , 46 ]. Oligoarthritis is also associated with DPB1*02 , DQB1*04 , DRB1*01 , DRB1*08 , DRB1*11 , and DRB1*13 [ 47 , 48 ]. DRB1*11:03/11:04 and DRB1*08:01 confer susceptibility to both oligoarthritis and polyarthritis RF-negative JIA patients [ 49 ].…”

Section: Genetic Studies Of Polygenic Forms Of Jiamentioning

confidence: 99%

The Multi-Omics Architecture of Juvenile Idiopathic Arthritis

Hou

Zhang

et al. 2020

Cells

View full text Add to dashboard Cite

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.

show abstract

Both HLA class II and class III DNA polymorphisms are linked to juvenile rheumatoid arthritis susceptibility

Cited by 23 publications

References 23 publications

EULAR recommendations for vaccination in paediatric patients with rheumatic diseases

EULAR recommendations for vaccination in paediatric patients with rheumatic diseases

B Cells on the Stage of Inflammation in Juvenile Idiopathic Arthritis: Leading or Supporting Actors in Disease Pathogenesis?

The Multi-Omics Architecture of Juvenile Idiopathic Arthritis

Contact Info

Product

Resources

About