TY - JOUR
T1 - Cytokine gene polymorphisms and susceptibility to juvenile idiopathic arthritis
AU - Donn, R. P.
AU - Barrett, J. H.
AU - Farhan, A.
AU - Stopford, A.
AU - Pepper, L.
AU - Shelley, E.
AU - Davies, N.
AU - Ollier, W. E R
AU - Thomson, W.
PY - 2001
Y1 - 2001
N2 - Objective. To investigate the involvement of candidate cytokine genes in the pathogenesis of juvenile idiopathic arthritis (JIA). Methods. Single nucleotide polymorphisms and intragenic microsatellite markers within 8 candidate cytokine genes (interleukin-1α [IL-1α], IL-2, IL-4, IL-6, IL-10, interferon-α1 [IFNA1], interferon-γ [IFNG], and interferon regulatory factor 1 [IRF-1]) were investigated in 417 Caucasian patients with clinically characterized JIA and a panel of 276 unrelated, healthy Caucasian controls, all from the United Kingdom. Results. A novel 3′-untranslated region (3′UTR) polymorphism in IRF-1 was found to be associated with susceptibility to JIA (corrected P = 0.002). No significant association with IL-1α, IL-2, IL-4, IL-6, IL-10, IFNA1, or IFNG was observed. Conclusion. An association between JIA and a previously unreported 3′UTR polymorphism of IRF-1 was observed. This association was not found to be specific to any particular JIA subgroup. This suggests that IRF-1 may contribute to a common pathogenesis shared by all JIA patients, regardless of clinical pheno-type. This is most likely to be a genetic contribution to the chronic inflammatory process that underlies JIA pathology.
AB - Objective. To investigate the involvement of candidate cytokine genes in the pathogenesis of juvenile idiopathic arthritis (JIA). Methods. Single nucleotide polymorphisms and intragenic microsatellite markers within 8 candidate cytokine genes (interleukin-1α [IL-1α], IL-2, IL-4, IL-6, IL-10, interferon-α1 [IFNA1], interferon-γ [IFNG], and interferon regulatory factor 1 [IRF-1]) were investigated in 417 Caucasian patients with clinically characterized JIA and a panel of 276 unrelated, healthy Caucasian controls, all from the United Kingdom. Results. A novel 3′-untranslated region (3′UTR) polymorphism in IRF-1 was found to be associated with susceptibility to JIA (corrected P = 0.002). No significant association with IL-1α, IL-2, IL-4, IL-6, IL-10, IFNA1, or IFNG was observed. Conclusion. An association between JIA and a previously unreported 3′UTR polymorphism of IRF-1 was observed. This association was not found to be specific to any particular JIA subgroup. This suggests that IRF-1 may contribute to a common pathogenesis shared by all JIA patients, regardless of clinical pheno-type. This is most likely to be a genetic contribution to the chronic inflammatory process that underlies JIA pathology.
KW - Support,Non-U.S.Gov't
U2 - 10.1002/1529-0131(200104)44:4<802::AID-ANR136>3.0.CO;2-G
DO - 10.1002/1529-0131(200104)44:4<802::AID-ANR136>3.0.CO;2-G
M3 - Article
SN - 2151-464X
VL - 44
SP - 802
EP - 810
JO - Arthritis Care & Research
JF - Arthritis Care & Research
IS - 4
ER -