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      Effects of immunosuppressive therapy with prednisolone on B and T lymphocyte function in patients with chronic type B hepatitis.

      Hepatology (Baltimore, Md.)
      Adult, B-Lymphocytes, drug effects, immunology, Clinical Trials as Topic, Dose-Response Relationship, Drug, Double-Blind Method, Female, Hepatitis B, drug therapy, Hepatitis, Chronic, Humans, Immunoglobulins, biosynthesis, Immunosuppression, Lymphocyte Activation, Male, Middle Aged, Mitogens, pharmacology, Prednisolone, therapeutic use, Random Allocation, T-Lymphocytes, T-Lymphocytes, Helper-Inducer, T-Lymphocytes, Regulatory

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          Abstract

          B and T lymphocyte function was studied in 10 patients with chronic type B hepatitis before, during and after a 28-day course of prednisolone therapy. Lymphocyte function was assessed by measuring the in vitro synthesis of immunoglobulin by peripheral blood mononuclear cells stimulated with pokeweed mitogen and by assaying lymphocyte proliferation in response to B and T cell mitogens. During high dose prednisolone therapy, there was a decrease in immunoglobulin synthesis by peripheral blood mononuclear cells and in lymphocyte proliferation to all mitogens. Studies using separated B and T cells showed that prednisolone treatment led to a decrease in both helper and suppressor T cell function but an enhancement of primary B cell function. When prednisolone was withdrawn, lymphocyte function rapidly returned to baseline levels. During prednisolone therapy, serum aminotransferase activities decreased by an average of 50%. In all patients, there was a subsequent rebound increase in serum aminotransferase activities 4 to 10 weeks after withdrawal of prednisolone. This was accompanied by a striking increase in suppressor T lymphocyte activity without significant changes in either helper T cell or B cell function. The close correlation between changes in helper and suppressor T lymphocyte function and serum aminotransferase activities during and after immunosuppressive therapy suggests that immunoregulatory T lymphocytes may play an important role in the pathogenesis of chronic type B hepatitis.

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