Hanson R G, Peters M G, Hoofnagle J H
Hepatology. 1986 Mar-Apr;6(2):173-9. doi: 10.1002/hep.1840060204.
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 When prednisolone was withdrawn, lymphocyte function rapidly returned to baseline levels.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.
对10例慢性乙型肝炎患者在接受为期28天的泼尼松龙治疗前、治疗期间及治疗后,研究了B淋巴细胞和T淋巴细胞的功能。通过检测用美洲商陆有丝分裂原刺激外周血单个核细胞后免疫球蛋白的体外合成情况,以及检测淋巴细胞对B细胞和T细胞有丝分裂原的增殖反应,来评估淋巴细胞功能。在高剂量泼尼松龙治疗期间,外周血单个核细胞的免疫球蛋白合成以及淋巴细胞对所有有丝分裂原的增殖反应均下降。对分离的B细胞和T细胞进行的研究表明,泼尼松龙治疗导致辅助性T细胞和抑制性T细胞功能均下降,但原发性B细胞功能增强。停用泼尼松龙后,淋巴细胞功能迅速恢复至基线水平。在泼尼松龙治疗期间,血清氨基转移酶活性平均下降了50%。在所有患者中,停用泼尼松龙后4至10周,血清氨基转移酶活性随后出现反弹性升高。这伴随着抑制性T淋巴细胞活性的显著增加,而辅助性T细胞或B细胞功能均无明显变化。免疫抑制治疗期间及之后,辅助性T淋巴细胞和抑制性T淋巴细胞功能的变化与血清氨基转移酶活性之间的密切相关性表明,免疫调节性T淋巴细胞可能在慢性乙型肝炎的发病机制中起重要作用。