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Cell Cycle Independent Lymphocytotoxicity of 2-Chlorodeoxyadenosine

  • Dennis A. Carson
  • Donald B. Wasson
  • Alice Yu
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 165)

Abstract

Deoxyadenosine and its nucleotides have been implicated in the pathogenesis of the immunodeficient state associated with an inherited deficiency of adenosine deaminase (ADA) (1,2), In ADA deficient patients, T lymphocytes may selectively phosphorylate deoxyadenosine released by other tissues. Both dividing and resting T cells have abundant deoxyadenosine phosphorylating activity, mediated primarily by deoxycytidine kinase, but minimal deoxynucleotide dephosphorylating activity, mediated by cytoplasmic deoxynucleotidase (3,4). For this reason, normal and malignant T lymphocytes exposed to micromolar concentrations of deoxyadenosine, in the presence of an ADA inhibitor, progressively accumulate dATP until cell death ultimately ensues (5,6).

Keywords

Adenosine Deaminase Lymphoblastoid Cell Line Cytosine Arabinoside Severe Combine Immunodeficiency Purine Nucleoside Phosphorylase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1984

Authors and Affiliations

  • Dennis A. Carson
    • 1
    • 2
  • Donald B. Wasson
    • 1
    • 2
  • Alice Yu
    • 1
    • 2
  1. 1.Department of Clinical ResearchResearch Institute of Scripps ClinicLa JollaUSA
  2. 2.Department of PediatricsUniversity of CaliforniaSan Diego, La JollaUSA

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