2008
DOI: 10.1136/ard.2007.083782
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Association between  2 adrenergic receptor polymorphisms and rheumatoid arthritis in conjunction with human leukocyte antigen (HLA)-DRB1 shared epitope

Abstract: There was a highly significant distortion between patients with RA and controls in the distribution of beta2AR polymorphisms at codon 16, contributing (together with the HLA-DR alleles) to the genetic background of RA.

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Cited by 28 publications
(30 citation statements)
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“…[8][9][10][11][12] Polymorphisms within ADRB2 were described in association with different disorders, including not only asthma and obesity but also hypertension, 13 autism, 14 cerebral palsy, 15 susceptibility to parasite infestation, 16 and rheumatoid arthritis. 17 The ADRB2 Gene…”
mentioning
confidence: 99%
“…[8][9][10][11][12] Polymorphisms within ADRB2 were described in association with different disorders, including not only asthma and obesity but also hypertension, 13 autism, 14 cerebral palsy, 15 susceptibility to parasite infestation, 16 and rheumatoid arthritis. 17 The ADRB2 Gene…”
mentioning
confidence: 99%
“…Responsivity of b 2 -ARs are affected by polymorphisms at positions 16 and 27, which determine the propensity for agonistinduced downregulation and associated subsensitivity (Green et al 1993(Green et al , 1995. According to genetic studies performed in northern Sweden (Xu et al 2005) and in Germany (Malysheva et al 2008), carriage of Arg16 and of Gln27 was associated with RA, carriage of Gln27 was associated with activity of the disease and in combination with non-carriage of Arg16 with higher levels of rheumatoid factor, and homozygosity for Arg16 exhibited the greatest risk for RA in combination with HLA-DRB1*04. Association of Arg16 and of Gln27 was not found in a population of children with JRA (Pont-Kingdon et al 2009).…”
Section: Rheumatoid Arthritismentioning
confidence: 98%
“…Les lymphocytes des patients atteints de PR sont notamment caractérisés par une moindre expression du récepteur ␤2 adrénergique, corrélée négativement à l'activité de la maladie. Chez des patients allemands atteints de PR, un polymorphisme responsable d'une mutation non synonyme du codon 16 (Arg16Gly), caractérisé par la substitution d'une arginine par une glycine, s'est avéré associé à la susceptibilité à la maladie, ainsi qu'à la positivité des ACPA (ACPA+ chez 93 % des homozygotes pour l'allèle encodant l'arginine contre 75 % des homozygotes pour l'allèle encodant la glycine) [28].…”
Section: Le Gène T-box 21 (22q112)unclassified