Our research in a rodent autoimmune model of RA supports that under chronic inflammation and autoimmunity, β2-AR signal transduction is altered in spleen cells and in disease-relevant lymph nodes [89,124], such that the β2-AR uses GRKs and β-arrestin pathways instead of cAMP-PKA to mediate spleen cells responses during the effector phase of inflammatory arthritis. This evidence concerns the gene ADRB2 and Autoimmunity.