Is there correlation of T cell proliferative functions and surface marker phenotypes in patients with acquired immune deficiency syndrome or lymphadenopathy syndrome?

We have investigated the respective role of quantitative T lymphocyte subset abnormalities, interleukin-2 (IL-2) production and responsiveness to IL-2, in the proliferative deficiency that is observed in acquired immune deficiency syndrome (AIDS) and Lymphadenopathy syndrome (LAS) patients or even in some apparently healthy male homosexuals. 83 subjects were evaluated: 35 symptom free male homosexuals (HC), 24 LAS and 24 AIDS patients. As expected, many HC and most patients presented with T lymphocyte subset imbalance. These quantitative defects were associated with decreased reactivity to PHA and reduced production of IL-2 by PHA stimulated lymphocytes. No correlation however could be found between these two functions and variations in the T lymphocyte subset distribution. On the other hand, PHA responsiveness appeared to closely depend on IL-2 activity. Addition of exogenous IL-2 to lymphocytes from patients with low proliferative responses, stimulated with suboptimal PHA concentration, enhanced proliferation in some but not all the cases. In most instances this increase never reached the levels observed with similarly treated cells from normal individuals. In these patients, the limited number of lymphocytes which express IL-2 receptors upon PHA stimulation may explain both low PHA reactivity and reduced IL-2 responsiveness. These data indicate some possible mechanisms of immunodeficiency in AIDS and LAS.