Peripheral lymphocytes from 36 patients were used to study pathogenetic mechanisms of development of atopic bronchial asthma (ABA), which are associated with regulatory dysfunction of T lymphocytes. Models of determining immunoregulatory lymphocytic subpopulations (CD4+ and CD8+) and assessing the function of concanavalin A-induced immunoregulatory lymphocytes indicated that the reception of the immune mediators IL-2 and alpha-interferon was impaired in ABA patients. The paper gives the data on a significant drastic decrease in cAMP concentrations and an increase in cAMP levels in the peripheral lymphocytes in the patients.
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