Springer Online Journal Archives 1860-2000
Abstract Since abnormal immune responsesin vivo may result from altered purine metabolism, we sought to delineate a potential role in humoral immunodeficiency for cells with specific adenosine membrane receptors. The purine nucleoside, adenosine, had been shown at low concentrationsin vitro to be capable of activating a subset of T lymphocytes to inhibit pokeweed mitogen (PWM)-driven IgG synthesis, while higher concentrations inhibited both IgG and IgM. Sixteen patients with common variable immunodeficiency and four patients with immunodeficiency with hyper-IgM were evaluated for the number of adenosine receptor cells in unfractionated mononuclear cells as well as T- and non-T-cell fractions. Theophylline-sensitive T cells, a subset of T lymphocytes which have been shown to be capable of suppressing immunoglobulin responsesin vitro, were also quantitated. Four of 16 patients with panhypogammaglobulinemia had clearly elevated levels of adenosine receptor cells. Two of these same individuals had low numbers of theophylline-sensitive cells, as did one patient with hyper-IgM. Only one person with variable immunodeficiency had increased theophylline-sensitive T cells. We found cases of clear-cut disparity between adenosine receptor and theophylline-sensitive cells. Furthermore, these markers segregated independently in both patients and normals. Finally, we assessed the effect of adenosine receptor cell removal onin vitro PWM-driven immunoglobulin synthesis. In none of the 20 patients tested did this cause a significant elevation of IgG or IgM production, nor did it have a consistent effect on cells from normals. Thus, while adenosine can be shown to profoundly alter immunoglobulin productionin vitro and some patients with humoral immunodeficiency have abnormal numbers of cells with adenosine receptors, we were unable to find evidence for a pathophysiologic role for these cells in immunoglobulin deficiency in humans.
Type of Medium: