“…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).…”