A2 Adenosine Receptors in Neutrophils from Healthy Volunteers and Patients with Rheumatoid Arthritis

At physiological concentrations, adenosine can modulate a variety of biological activities by engaging specific cells surface receptors, termed A1 and A2, with different affinity for adenosine and adenosine analogues 1. Engagement of A2 adenosine receptors induces an increase in cAMP levels in several cells types, in contrast stimulation of A1 receptors causes opposite effects 2. It has been shown that adenosine and its analogues inhibit O2 generation 3, 4, phagocytosis and adherence by occupancy of specific adenosine A2 receptors, while the occupancy of A1 adenosine receptors enhance chemiotaxis 5, phagocytosis and adherence 6. In general, activation of adenosine receptors on leukocytes reduces immune and inflammatory responses7. Therefore, it may be suggested that release of adenosine is one mechanism by which normal cells protect themselves from activated neutrophils. Since it is possible that a decreased adenosine receptor functions are implicated in diseases like rheumatic pathologies characterised by an excess of inflammation. In the present report we described characteristics of adenosine binding sites on human neutrophils from healthy volunteers and rheumatic patients afflicted with rheumatoid arthritis by using [3 H]N ethylcarboxamidoadenosine (NECA) and [3 H] 2-p-(2-carboxyethyl) phenethylamino 5’ N-ethylcarboxamidoadenosine (CGS 21680) as ligands.