[Immunoregulatory disorders in chronic sinusitis in patients with atopy].
UNLABELLED: Disorders of immunoregulatory activity of T lymphocytes and excessive immunogenic activity of antigen presenting cells are recognised as an important pathogenic elements in allergic diseases. Successful prevention of development of these pathomechanisms determines the effectiveness of administered therapy. The aim of presented investigations was to assess the kind and the degree of immune disorders in the group of 40 patients with chronic allergic sinusitis (CAS). The range of evaluated parameters comprised the indices of immune competence of T cells in microcultures of mononuclear cells isolated from the blood (response to mitogens PHA and Con A, saturation of IL-2 receptors, T-cell suppressive activity--SAT index), indices of immunogenic activity of monocytes (LM index correlated with the ratio of concentrations of IL-1 beta/IL-1ra, concentrations of IL-1beta, IL-1ra, IL-4 and IL-6 in the culture supernatants). The results were compared with the similar estimations performed in the group of 20 healthy blood donors. RESULTS: The obtained results demonstrated significant deficiency of T cell immune competence in the group of patients suffering from CAS (hyperreactivity of non-matured T cells to Con A, decreased saturation of IL-2 receptors, deficient T-cell suppressive activity and quantitative deficiency of TCD8 cells). In contrast to that, the immunogenic activity of monocytes was significantly elevated in the group of CAS patients as compared to the control group (significantly higher values of LM index, considerable increased concentrations of IL-1b, IL-4 and IL-6). CONCLUSIONS: The observed immunoregulatory deficiency of T-cell population and increased immunogenic activity of antigen presenting cells (monocytes) in CAS patients seem to suggest that the routine antiinflammatory treatment in these patients should be supplemented with the immunocorrective therapy aimed to restore the deficient thymus-dependent immune competence.