The CD39-adenosinergic axis in the pathogenesis of immune and nonimmune diabetes

Abstract

Diabetes mellitus encompasses two distinct disease processes: autoimmune Type 1 (T1D) and nonimmune Type 2 (T2D) diabetes. Despite the disparate aetiologies, the disease phenotype of hyperglycemia and the associated complications are similar. In this paper, we discuss the role of the CD39-adenosinergic axis in the pathogenesis of both T1D and T2D, with particular emphasis on the role of CD39 and CD73.

Figure 1

Mice deficient in CD73 are resistant to MLDS-induced diabetes. Diabetes incidence in C57BL/6 wild-type (WT) mice (black squares, n = 4) and CD73KO (black triangles, n = 8) mice following MLDS. **P < 0.01 versus WT mice.

Figure 2

Inhibition of A2B receptor in CD73KO mice increases susceptibility to MLDS-induced diabetes. Diabetes incidence of CD73KO mice treated with either saline (open triangles, n = 6) or the A2BR inhibitor (dose: 0.5 μg/g body weight (BW), twice daily) (black triangles, n = 6). *P < 0.05 versus saline-treated mice.

Figure 3

Normal glucose handling in CD73KO mice. Blood glucose levels following 1 mg/g BW of intraperitoneal glucose. WT mice (black squares, n = 6); CD73KO mice (black triangles, n = 8); ns—not significant versus WT mice.