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Rheumatoid arthritis (RA) is characterized by inflammation of the synovium, which leads to the progressive destruction of cartilage and bone. Adrenoreceptor (AR) signaling may play an important role in modulating dendritic cell (DC), which may be involved in the pathogenesis of RA. We examined the effect of the β-AR agonist isoprenaline (ISO) on DC function, the impact of the β 2 -AR agonist salbutamol on adjuvant-induced arthritic (AA) rats, and changes in β 2 -AR signaling in DCs during the course of AA. ISO inhibited the expression of the surface molecules CD86 and MHC-II, inhibited the stimulation of T lymphocyte proliferation by DC and TNF-α secretion, and promoted DC antigen uptake and IL-10 secretion. The effects of ISO on MHC-II expression, DC stimulation of T lymphocyte proliferation, and DC antigen uptake were mediated by β 2  - AR. Treatment with salbutamol ameliorated the severity of AA and histopathology of the joints and inhibited proliferation of thymus lymphocytes and FLS  in vivo.  β 2 -AR signaling was weaker in AA rats compared to the control. Elevated GRK2 and decreased β 2 -AR expression in DC cytomembranes were observed in AA and may have decreased the anti-inflammatory effect of β 2 -AR signaling. Decreased β 2 -AR signaling may be relevant to the exacerbation of arthritis inflammation.

β2-adrenoceptor signaling reduction in dendritic cells is involved in the inflammatory response in adjuvant-induced arthritic rats