作者: T. Hovi
DOI: 10.1007/978-94-011-6197-8_10
关键词:
摘要: Proliferation of antigen-sensitized lymphocytes is one the basic phenomena in immune response. Several lines evidence suggest that proliferation relatively sensitive to changes purine metabolism1,2. Hereditary deficiencies either adenosine deaminase (ADA) or nucleoside phosphorylase (PNP), enzymes pathways responsible for degradation nucleotides and nucleosides, result severe immunodeficiency diseases leaving functions most other tissues almost unaffected3,4. The failure system ADA deficiency seems be based on accumulation adenosine, substrate ADA, its metabolic products tissues3,5,6. This hypothesis supported by findings exposure normal mitogen-stimulated lymphocyte cultures exogenous can inhibit cells7-9. Molecular mechanisms this inhibition are not known, but several alternatives have been suggested, all which approached experimentally9-11.