Immunological aspects of purine metabolism.
Adv Exp Med Biol, 1977;76A:412-33.
Seegmiller JE, Watanabe T, Shreier MH, Waldmann TA
PMID: 193375
Impact factor: 3.65
Abstract
The development of our knowledge of the immune system has been reviewed and evidence presented of the need for a rapid rate of purine synthesis de novo for the proliferative events in this process. The mechanism of the inhibition of the immune system in a model of ADA deficiency has been studied intensively and considerable indirect evidence obtained of adenosine toxicity as a possible mediator of a reversible inhibition of proliferation of T-cells and to a slightly lesser extent B-cells. A secondary inhibition of ADA by inosine accumulation in PNP deficiency is proposed as a unifying hypothesis in which a somewhat lesser adenosine toxicity would inhibit proliferation only only of T-cells. The correction of the immune response by addition of ADA both in vitro and in vivo provides strong evidence in favor of this view. In HPRT deficiency no evidence was found of a gross impairment of the immune system; however, the HPRT enzyme is required for inhibition of the immune response by 6MP in a variety of systems using different mitogenic stimuli.
MeSH terms
Adenine; Adenosine; Adenosine Deaminase; Antibody Formation; Hormones; Humans; Immunity, Cellular; Immunologic Deficiency Syndromes; Immunosuppression Therapy; Inosine; Lesch-Nyhan Syndrome; Liver; Lymphocyte Activation; Lymphocytes; Mercaptopurine; Models, Biological; Nucleoside Deaminases; Pentosyltransferases; Purine-Nucleoside Phosphorylase; Purines; Synaptic Transmission; Uridine
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