The purine metabolic enzymes adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) are important in lymphocyte differentiation, and genetic deficiencies of either enzyme have been associated with hereditary immunodeficiency states. Both ADA and PNP activity were measured in null cell-enriched and T cell-enriched peripheral blood lymphocytes from 16 patients with the acquired immune deficiency syndrome (AIDS), seven patients with the AIDS-related symptom complex (ARC), and seven asymptomatic homosexuals. ADA activity in nmol/106 lymphocytes/h was significantly elevated in null lymphocytes from AIDS (161 ± 12) as compared with 23 healthy heterosexual controls (127 ± 8; P < .025). PNP activity was also significantly increased in null lymphocytes from AIDS patients (96 ± 10; P < .005) as well as those from ARC patients (84 ± 11; P < .025) relative to controls (61 ± 5). No significant differences in enzyme activity were noted in T cell-enriched cells in any group. Along with elevated enzyme activity, AIDS patients had small yet significant increases in the percentages of HLA-DR (P < .025), terminal deoxynucleotidyl transferase (TdT) (P < .0001), and peanut agglutinin receptor (P < .0001) positive lymphocytes in the null fraction compared with controls. TdT-positive cells appeared morphologically as large lymphoblasts with irregular nuclei. The data imply that the cellular immune deficiency in AIDS is not a result of deficiencies in lymphocyte ADA or PNP activity, but is more likely associated with an increase in an immature and/or activated lymphocyte subset.
|Original language||English (US)|
|Number of pages||7|
|State||Published - 1985|
ASJC Scopus subject areas
- Cell Biology