作者: Lawrence M. Lichtenstein , Gianni Marone , Marshall Plaut
DOI: 10.1007/BF02905345
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摘要: In the past several years study of primary immunodeficiencies has led to an explosive growth basic information on pathophysiology immune system. 1972 a deficiency adenosine deaminase (ADA) was described in two patients with severe combined immunodeficiency (SCID). Shortly thereafter, deficiencies other enzymes involved purine salvage pathway (i.e., nucleoside phosphorylase and ecto-5′-nucleotidase) were association, respectively, defective T- B-lymphocyte activity. Although exact biochemical mechanism(s) these is not known, elevated levels adenosine, 2-deoxyadenosine their metabolites occur patients. Adenosine inhibitsin vitro lymphocyte proliferation, T-lymphocyte-mediated cytolysis, monocyte chemotaxis basophil histamine release. We have found that increases cAMP levels, by interacting specific plasma membrane receptor which leads activation adenylate cyclase. also explored influence control release from human basophils shown inhibits IgE-mediated reaction. The action appears be mediated cell-surface receptor. plays central complex role transmethylation reactions. These reactions modulate inflammatory reactions, including chemotaxis, mitogenesis, probably basophils. Thus, may act as endogenous modulator function separate but interrelated effects: its ability interact receptor, and/or intracellular methylation.