The cellular basis for viral-induced immunodeficiency: analysis by monoclonal antibodies.
The cellular basis for viral-induced immunodeficiency: analysis by monoclonal antibodies.
复制标题
病毒引起的免疫缺陷的细胞基础：单克隆抗体分析。
作者：
E. Reinherz;C. O'brien;P. Rosenthal;S. Schlossman
病毒感染通常与免疫缺陷状态有关。虽然T淋巴细胞被认为抑制宿主的反应，但确切的病因仍不清楚。因此，我们用单克隆抗体（滴度10（-5）至10（-7））鉴定了6名传染性单核细胞增多症（IM）急性期和恢复期患者的T淋巴细胞，这些单克隆抗体的抗原仅限于TH 2辅助（T4）和TH 2抑制（T5）T细胞亚群以及常见的T细胞抗原（T3）和HLA-D相关Ia抗原。发现在急性传染性单核细胞增多症期间，存在抑制性T细胞（T5+，Ia+表型）的活化和增加。在功能上，急性IM淋巴细胞抑制自体T细胞增殖抗原以及美洲商陆有丝分裂原驱动的B细胞免疫球蛋白的生产。相反，恢复期与T细胞亚群和免疫功能恢复正常有关。这些结果表明，病毒感染可以优先激活特定的T细胞亚群，并抑制整个人体免疫反应。
Viral infections are often associated with immunodeficiency states. Although T lymphocytes have been thought to suppress the host's response, the precise etiology remains unclear. Therefore, we characterized T lymphocytes from six patients during both acute and convalescent phases of infectious mononucleosis (IM) with monoclonal antibodies (titer, 10(-5) to 10(-7) to antigens restricted to the TH2- helper (T4) and TH2 suppressor (T5) T cell subsets as well as to a common T cell antigen (T3) and HLA-D related Ia antigens. It was found that during acute infectious mononucleosis, there is both activation and increase of suppressor T cells (T5+, Ia+ phenotype). Fuctionally, the acute IM lymphocytes suppress autologous T cell proliferation to antigens as well as pokeweed mitogen driven B cell immunoglobulin production. In contrast, convalescence is associated with a return to normal of T cell subsets and immune function. These results demonstrate that viral infections can preferentially activate a specific T cell subset and suppress the overall human immune response.