LYMPHOCYTES AND LMYPHOKINES IN APLASTIC ANEMIA

以前的研究表明，再生障碍性贫血患者的血清中 活化的抑制性淋巴细胞（细胞表面表型Leu 2+， Tac+，HLA-DR+），过度产生γ-干扰素（g-IFN），淋巴因子 负责体外和可能体内的造血抑制。 T细胞抗原受体基因重排的分子特征 已经表明，异常的抑制细胞群体不是克隆的， 起源 干扰素的抑制潜力被进一步阐明， 使用纯重组干扰素（r-IFN）。 虽然r-IFN直接 抑制造血祖细胞，少量之间的协同作用 γ干扰素和α干扰素的增加需要 辅助细胞的存在。 ATG和ALG的抗体特异性 以更好地定义这些制剂。 ATG和ALG均为 发现含有针对几种T细胞抗原的抗体; 但活性ATG和ALG之间无显著差异 批次和体内活性较低的ALG批次。 淋巴细胞亚群及 再生障碍性贫血患者的淋巴因子的产生进行了研究， 后ATG。 尽管在总的或抑制因子方面没有显著变化， ATG后的淋巴细胞，携带白细胞介素2的淋巴细胞数量 所有对治疗有反应的患者的受体均降至正常范围; 相比之下，60%的无应答者的Tac抗原仍然增加， 表情 在研究的3例患者中，这种减少发生在抑制因子上， 而不是辅助淋巴细胞。外周血和外周血中的干扰素水平 9例患者中8例骨髓血清降低，1例无骨髓抑制， 减少是无应答者。 这些结果是一致的 再生障碍性贫血的病因有哪些？ ATG后消除的活化抑制细胞群 疗法

Previous work has shown that patients with aplastic anemia have an elevated number of activated suppressor lymphocytes (cell surface phenotype Leu 2+, Tac+, HLA-DR+) that overproduce gamma-interferon (g-IFN), the lymphokine responsible for hematopoietic suppression in vitro, and possibly in vivo. Molecular characterization of T cell antigen receptor gene rearrangements has shown that the abnormal suppressor cell population is not clonal in origin. The inhibitory otential of interferons was further clarified by the use of pure recombinant interferons (r-IFNs). Though r-IFNs directly inhibited hematopoietic progenitor cells, the synergy between small amounts of gamma interferon and increasing amounts of alpha interferon required the presence of auxiliary cells. The antibody specificities in ATG and ALG were evaluated to better define these preparations. Both ATG and ALG were found to contain antibodies directed against several T cell antigens; however no significant differences were seen between active ATG and ALG lots and an ALG lot with less activity in vivo. Lymphocyte subsets and lymphokine production from aplastic anemia patients were studied pre- and post-ATG. Though there was not a significant change in total or suppressor lymphocytes after ATG, the number of lymphocytes bearing the interleukin 2 receptor fell to the normal range in all patients who responded to therapy; in contrast, 60% of nonresponders still had increased Tac antigen expression. In 3 patients studied, this decrease occurred on suppressor but not helper lymphocytes. Interferon levels in the peripheral blood and bone marrow sera decreased in 8/9 patients; the 1 patient without a decrease was a nonresponder. These results are consistent with the hypothesis that some cases of aplastic anemia are caused by an abnormal population of activated suppressor cells which are eliminated after ATG therapy.