The Role ofde novoPurine Synthesis in Lymphocyte Transformation

Autor: R. W. E. Watts, A. C. Allison, A. D. B. Webster, T. Hovi
Rok vydání: 2008
Předmět:
Zdroj: Ciba Foundation Symposium 48-Purine and Pyrimidine Metabolism ISBN: 9780470720301
Ciba Foundation Symposium 48 - Purine and Pyrimidine Metabolism
DOI: 10.1002/9780470720301.ch13
Popis: Genetic defects in purine metabolism are associated with severe immunodeficiency. Adenosine deaminase deficiency impairs the function of both B- and T-lymphocytes whereas in purine nucleoside (inosine) phosphorylase deficiency there is more severe impairment of T-lymphocyte functions than of B-lymphocyte functions. The relative unimportance of the salvage pathway catalysed by hypoxanthine-guanine phosphoribosyltransferase is shown by the normal responses of T-lymphocytes from patients with the Lesch-Nyhan syndrome to antigenic and mitogenic stimulation. A mild deficiency of B-lymphocyte function is found in these patients. Agents inhibiting the de novo pathway of purine synthesis, including azaserine, 6-mercaptopurine and azathioprine in low doses, block the responses of normal human lymphocytes to mitogenic stimulation. These observations emphasize the importance of the de novo pathway of purine synthesis in lymphocyte responses to antigenic and mitogenic stimulation. There is considerable heterogeneity in the amount of labelled uridine incorporated into human and rat lymphocytes. This does not appear to reflect only a difference between T- and B-lymphocytes
Databáze: OpenAIRE