Role of suppressor T cells in pathogenesis of common variable hypogammaglobulinaemia.
Role of suppressor T cells in pathogenesis of common variable hypogammaglobulinaemia.
复制标题
抑制性 T 细胞在常见变异低丙种球蛋白血症发病机制中的作用。
DOI：
10.1016/s0140-6736(74)91940-0
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发表时间：
1974
期刊：
影响因子：
168.9
通讯作者：
W. Strober
中科院分区：
文献类型：
--
作者：
T. Waldmann;S. Broder;R. Blaese;M. Durm;M. Blackman;W. Strober
使用一种研究B淋巴细胞向免疫球蛋白合成和分泌细胞的终末分化的技术，研究了常见变异性低丙种球蛋白缺乏症患者的缺陷性质。正常人外周血淋巴细胞的几何平均合成率为1641 ng。对于免疫球蛋白，1698 ng。Ig A和3715 ng。在商陆有丝分裂原存在下培养7天，每2×106个细胞的IgM。相比之下，所研究的所有13名低丙种球蛋白缺乏症患者的淋巴细胞都合成并分泌不到100毫微克。在此期间，每一类免疫球蛋白的数量。8例低丙种球蛋白血症患者中5例与正常淋巴细胞和商陆有丝分裂原共培养时，正常淋巴细胞合成免疫球蛋白的抑制率为84%~100%。当正常淋巴细胞与1例低丙种球蛋白缺乏症患者的胸腺来源淋巴细胞(T细胞)共同培养时，观察到正常淋巴细胞对免疫球蛋白合成的抑制作用。在对照研究中，当正常细胞与来自无关正常个体或Sezary综合征患者的淋巴细胞共同培养时，免疫球蛋白合成没有被抑制，当它们与来自正常个体的纯化T细胞孵育时也没有被抑制。此外，正常淋巴细胞在低丙种球蛋白缺乏症患者的血清中培养时，免疫球蛋白合成没有受到抑制。这些研究表明，在一些患者中，常见的变量低丙种球蛋白缺乏症可能是由调节性T细胞的异常引起或持续的，调节性T细胞抑制B细胞的成熟和抗体的产生。
The nature of the defect in patients with common variable hypogammaglobulinæmia has been investigated using a technique established to study terminal differentiation of B lymphocytes into immunoglobulin synthesising and secreting cells. The peripheral-blood lymphocytes from normal individuals had geometric mean synthetic rates of 1641 ng. for IgG, 1698 ng. for IgA, and 3715 ng. for IgM per 2×106cells when cultured for seven days in the presence of pokeweed mitogen. In contrast, the lymphocytes from all 13 patients with hypogammaglobulinæmia studied synthesised and secreted less than 100 ng. of each class of immunoglobulin during this period. When lymphocytes from 5 of the 8 hypogammaglobulinæmic patients studied were co-cultured with normal lymphocytes and pokeweed mitogen, the synthesis of immunoglobulin by normal lymphocytes was depressed by 84 to 100%. A comparable suppression of immunoglobulin synthesis by normal lymphocytes was observed when they were co-cultured with purified thymus-derived lymphocytes (T cells) from a hypogammaglobulinæmic patient. In control studies, suppression of immunoglobulin synthesis was not seen when normal cells were co-cultured with lymphocytes from unrelated normal individuals or from patients with the Sezary syndrome, nor were they inhibited when incubated with purified T cells from normal individuals. In addition, no suppression of immuno-globulin synthesis by normal lymphocytes was observed when they were cultured in serum from the hypogammaglobulinæmic patients. Theses studies suggest that in some patients the disease common variable hypogammaglobulinæmia may be caused or perpetuated by an abnormality of regulatory T cells which act to suppress B-cell maturation and antibody production.