通过淋巴因子活性测定毒物对T细胞亚群的影响。

Effects of toxicants on T-cell subpopulations as determined by lymphokine activity.

作者信息

Archer D L, Smith B G, Johnson H M

出版信息

Arch Toxicol Suppl. 1980;4:138-42. doi: 10.1007/978-3-642-67729-8_29.

Abstract

Selective depletion of T1 and T2 lymphocyte subpopulations of mouse spleens was accomplished by injecting mice subcutaneously with 5 mg cortisone acetate (CA) or 0.1 ml antithymocyte serum (ATS), respectively. Selectively depleted and control spleen cells were cultured in vitro and were tested for their ability to produce the lymphokine immune interferon (IIF) in response to the following mitogens: staphylococcal enterotoxin A (SEA), concanavalin A (ConA), and phytohaemagglutinin-P (PHA). The data indicate that SEA and PHA induce IIF from T1 and T2 cells respectively; ConA induces IIF from both T1 and T2 cells. Mice were also injected subcutaneously with 10 mg gallic acid (GA) and the pattern of mitogen-induction of IIF from GA-treated spleen cells was compared with that of CA- and ATS-treated spleen cells. GA pretreatment of mice, like CA pretreatment, resulted in a significant decrease in SEA-induced IIF; GA probably exerts its effect on T1 suppressor cells.

摘要

分别给小鼠皮下注射5毫克醋酸可的松（CA）或0.1毫升抗胸腺细胞血清（ATS），实现对小鼠脾脏T1和T2淋巴细胞亚群的选择性耗竭。对选择性耗竭的和对照脾细胞进行体外培养，并检测它们在响应以下促细胞分裂剂时产生淋巴因子免疫干扰素（IIF）的能力：葡萄球菌肠毒素A（SEA）、刀豆球蛋白A（ConA）和植物血凝素-P（PHA）。数据表明，SEA和PHA分别从T1和T2细胞诱导产生IIF；ConA从T1和T2细胞均诱导产生IIF。给小鼠皮下注射10毫克没食子酸（GA），并将GA处理的脾细胞中促细胞分裂剂诱导IIF的模式与CA和ATS处理的脾细胞进行比较。小鼠经GA预处理后，与经CA预处理一样，SEA诱导的IIF显著降低；GA可能对T1抑制细胞发挥作用。