Table 1.
Demographic and clinical characteristics of kidney transplant recipients classified by presence kidney acute rejection.
Table 2.
Frequencies of the ENPP1 K121Q polymorphism between kidney transplant patients with acute rejection (AR) and without acute rejection (non-AR).
Fig 1.
Cox regression analysis of the ENPP1 K121Q polymorphism and acute rejection (AR) episodes in kidney transplant recipients.
Adjusted for HLA-DR, pregnancies, blood transfusions, recipient age, delayed graft function, and induction therapy.
Table 3.
Multivariate Cox regression analysis of risk factors for AR.
Fig 2.
(A) Ectonucleotidases cascade–Members of the NTPDase (CD39) family are cell membrane enzymes that hydrolyze ATP into ADP as well as ADP into AMP through three different steps. In contrast, NPPs are able to degrade ATP and ADP into AMP in a single step, releasing AMP. In the final hydrolyzation step, the extracellular AMP can then be hydrolyzed to adenosine and inorganic phosphate (Pi) by the effect of Ecto-5′-nucleotidase (CD73). (B) Regulation of immunity by ectonucleotidase cascade–The occurrence of pathological insults, such as AR, activates T cell receptors (TCR) expressed in T regulatory cells (Treg), which induces CD39/CD73 activity leading to adenosine generation. Increased levels of extracellular adenosine promote immunosuppressive and anti-inflammatory activity in Treg cells. Also, through its receptor A2A in the T effector cell, adenosine suppresses T cell immunity by inhibiting activation of T effector cells. Thus, by employing different mechanisms on Treg and T effector cells, adenosine promotes an immunosuppressive effect.