Article discusses the sensitivity of CD73-deficient mice to collagen-induced arthritis. We demonstrated that CD73, which participates in the formation of extracellular adenosine, plays a protective role in the development of collagen-induced arthritis (CIA).
Modulation of adenosine signaling is a promising new approach for treatment of RA. Our study provides the first evidence that CD73 expression is a homeostatic mechanism that downmodulates joint inflammation.
Our data also confirm the protective role of the A2A adenosin receptor in CIA in addition to the established protective role of the adenosine A3 receptor in this disease. Modulation of the CD 73-adenosinergic pathway may thus constitute a promising approach for tteatment of RA.