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. 2013 Dec 15;1(2):79–86. doi: 10.14218/JCTH.2013.00015

Fig. 2. Pathogenesis of liver attack in AIH: the role of CD39.

Fig. 2

In health, immunotolerance to liver autoantigens is maintained by effective control of CD4+CD25+FOXP3+Tregs over CD4+ and CD8+ autoreactive T lymphocytes. The machinery enabling Tregs to modulate effector immune responses relies on the expression of CD39, an ectonucleotidase ultimately leading to the generation of immunomodulatory adenosine. In AIH, Tregs are numerically defective and express low levels of CD39. This results in poor generation of adenosine and ineffective control over autoreactive lymphocytes, with consequent perpetuation of hepatocyte damage. Details of Treg adenosinergic suppression are depicted in the box. Adenosine is generated from ATP through the action of CD39 and CD73 ectonucleotidases in tandem, expressed by Tregs. Adenosine mediates immunomodulation by binding to A2A adenosine receptors on autoreactive T lymphocytes.