Abstract
While ADA is a ubiquitous enzyme in the purine degradation pathway. Surprisingly, inherited deficiency in ADA in human, results in a specific severe combined immunodeficiency decease, where the tissue damage is restricted to the lymphoid lineage.1 Previous studies have demonstrated that during T lymphocyte development ADA activity peaks at immature cortical CD4+CD8+ double positive (DP) thymocytes.2,3
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Cohen, A., Zhu, W., Benveniste, P. (1998). Role Of Adenosine Deaminase and dATP Levels in Thymocyte Apoptosis. In: Griesmacher, A., Müller, M.M., Chiba, P. (eds) Purine and Pyrimidine Metabolism in Man IX. Advances in Experimental Medicine and Biology, vol 431. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5381-6_81
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DOI: https://doi.org/10.1007/978-1-4615-5381-6_81
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