PMID- 31169548
OWN - NLM
STAT- MEDLINE
DCOM- 20200525
LR  - 20210410
IS  - 1531-6963 (Electronic)
IS  - 1040-8711 (Print)
IS  - 1040-8711 (Linking)
VI  - 31
IP  - 5
DP  - 2019 Sep
TI  - Implications of juvenile idiopathic arthritis genetic risk variants for disease 
      pathogenesis and classification.
PG  - 401-410
LID - 10.1097/BOR.0000000000000637 [doi]
AB  - PURPOSE OF REVIEW: We assess the implications of recent advances in the genetics 
      of juvenile idiopathic arthritis (JIA) for the evolving understanding of 
      inflammatory arthritis in children. RECENT FINDINGS: JIA exhibits prominent 
      genetic associations with the human leukocyte antigen (HLA) region, extending 
      perhaps surprisingly even to the hyperinflammatory systemic JIA category. Some 
      HLA associations resemble those for adult-onset inflammatory arthritides, 
      providing evidence for pathogenic continuity across the age spectrum. Genome-wide 
      association studies have defined an increasing number of JIA-linked non-HLA loci, 
      many again shared with adult-onset arthritis. As most risk loci contain only 
      noncoding variants, new experimental methods such as SNP-seq and innovative 
      big-data strategies help identify responsible causative mutations, termed 
      functional SNPs (fSNPs). Alternately, gene hunting in multiplex families 
      implicates new genes in monogenic childhood arthritis, including MYD88 and the 
      intriguing innate immune gene LACC1. SUMMARY: Genetic data indicate a continuity 
      between JIA and adult arthritis poorly reflected in current nomenclature. 
      Advancing methodologies will help to identify new pathogenic mechanisms that 
      inform the understanding of biologic subdivisions within JIA. Resulting insights 
      will facilitate the application of lessons learned across the age spectrum to the 
      treatment of arthritis in children and adults.
FAU - Nigrovic, Peter A
AU  - Nigrovic PA
AD  - Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital.
AD  - Division of Immunology, Boston Children's Hospital, Harvard Medical School, 
      Boston, Massachusetts.
FAU - Martinez-Bonet, Marta
AU  - Martinez-Bonet M
AD  - Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital.
AD  - Instituto de Investigacion Sanitaria Gregorio Maranon, Madrid, Spain.
FAU - Thompson, Susan D
AU  - Thompson SD
AD  - Center for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital 
      Medical Center, Department of Pediatrics, University of Cincinnati, Cincinnati, 
      Ohio, USA.
LA  - eng
GR  - R01 AR073201/AR/NIAMS NIH HHS/United States
GR  - P30 AR070253/AR/NIAMS NIH HHS/United States
GR  - R01 AR065538/AR/NIAMS NIH HHS/United States
GR  - P30 AR070549/AR/NIAMS NIH HHS/United States
GR  - R01 AR075906/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Curr Opin Rheumatol
JT  - Current opinion in rheumatology
JID - 9000851
RN  - 0 (HLA Antigens)
SB  - IM
MH  - Arthritis, Juvenile/*genetics
MH  - *Genetic Predisposition to Disease
MH  - Genome-Wide Association Study/*methods
MH  - HLA Antigens/*genetics
MH  - Humans
MH  - *Polymorphism, Single Nucleotide
MH  - Risk Factors
PMC - PMC6800096
MID - NIHMS1054690
EDAT- 2019/06/07 06:00
MHDA- 2020/05/26 06:00
PMCR- 2020/09/01
CRDT- 2019/06/07 06:00
PHST- 2019/06/07 06:00 [pubmed]
PHST- 2020/05/26 06:00 [medline]
PHST- 2019/06/07 06:00 [entrez]
PHST- 2020/09/01 00:00 [pmc-release]
AID - 10.1097/BOR.0000000000000637 [doi]
PST - ppublish
SO  - Curr Opin Rheumatol. 2019 Sep;31(5):401-410. doi: 10.1097/BOR.0000000000000637.