REGULATION OF HUMAN T CELL RESPONSES BY ADHERENT CELLS

Leu M3+人外周血白细胞（PBL）耗竭 细胞粘附在塑料和葡聚糖凝胶G10上， 消除增殖性（3H）和细胞毒性T淋巴细胞（CTL） 对甲型流感病毒（FLU）的反应，但在3H 和对HLA同种异体抗原的CTL应答（ALLO）。 这一损失的 升高对HLA同种异体抗原（ALLO）的3H和CTL应答。 这种FLU T细胞应答的丧失归因于FLU T细胞的去除。 抗原呈递细胞（APC），而 ALLO反应显示是由于抑制细胞（或 抑制诱导细胞），其包含在Leu M3+粘附细胞中 细胞群 通过培养使抑制剂活性失活 未分级分离的PBL或带有病毒的贴壁细胞， 包括甲型流感、麻疹和腮腺炎病毒。

Depletion of human peripheral blood leukocytes (PBL) of Leu M3+ cells by adherence to plastic and sephadex G10 results in the abrogation of proliferative (3H) and cytotoxic T lymphocyte (CTL) responses to influenza A virus (FLU), but in an elevation of 3H and CTL responses to HLA alloantigens (ALLO). This loss of the elevation of 3H and CTL responses to HLA alloantigens (ALLO). This loss of the FLU T cell response was attributed to removal of antigen-presenting cells (APC), whereas the elevation of the ALLO response was shown to be due to suppressor cell (or a suppressor inducer cell) that is contained in the Leu M3+ adherent cell population. Suppressor activity was inactivated by culturing either unfractionated PBL or adherent cells with viruses, including influenza A, measles and mumps viruses.