Toxic-shock-syndrome toxin 1-induced proliferation of lymphocytes: comparison of the mitogenic response of human, murine, and rabbit lymphocytes.

Toxic-shock-syndrome toxin 1-induced proliferation of lymphocytes: comparison of the mitogenic response of human, murine, and rabbit lymphocytes.
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中毒性休克综合征毒素 1 诱导的淋巴细胞增殖:人、鼠和兔淋巴细胞促有丝分裂反应的比较。

DOI:
10.1093/infdis/151.1.65
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发表时间:
1985
期刊:
The Journal of infectious diseases
影响因子:
--
通讯作者:
P. Schlievert
P. Schlievert
中科院分区:
--
文献类型:
--
作者:
Nancy J. Poindexter;P. Schlievert

文献摘要

被引文献

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由金黄色葡萄球菌产生的毒性休克综合征毒素1(TSST 1)诱导从兔脾、小鼠脾、人外周血和脐带血中分离的淋巴细胞的体外增殖。这种促有丝分裂反应在所有三个系统中都是非特异性的。在小鼠和人类系统中,增殖依赖于响应淋巴细胞群中巨噬细胞的存在。由于无法从兔脾细胞悬液中去除巨噬细胞,因此无法确定该细胞在兔脾细胞增殖中的作用。TSST 1诱导的有丝分裂原性的动力学分析表明,淋巴细胞的增殖是最大的第4和第6天之间,在每一个检查的三个系统。每种系统对TSST 1的敏感性相似,在TSST 1剂量低至0.1 ng/5 × 10(5)鼠脾细胞或2 × 10(5)兔脾细胞和0.01 ng/3 × 10(5)人外周血单核细胞时达到最大增殖。对来自人外周血的小鼠脾细胞和单核细胞的分离群体的研究表明,TSST 1诱导的增殖反应仅存在于T细胞群体中。
Toxic-shock-syndrome toxin 1 (TSST 1) produced by Staphylococcus aureus induced in vitro proliferation of lymphocytes isolated from rabbit spleens, murine spleens, and both human peripheral blood and cord blood. This mitogenic response was nonspecific in all three systems. In the mouse and human systems, proliferation depended upon the presence of macrophages in the responding lymphocyte population. Inability to remove macrophages from rabbit splenocyte suspensions made it impossible to determine the contribution of this cell in rabbit splenocyte proliferation. Kinetic analysis of TSST 1-induced mitogenicity showed that proliferation of lymphocytes was maximal between days 4 and 6 in each of the three systems examined. Sensitivity to TSST 1 was similar in each system, with maximal proliferation achieved at TSST 1 doses as low as 0.1 ng/5 X 10(5) murine splenocytes or 2 X 10(5) rabbit splenocytes, and 0.01 ng/3 X 10(5) human mononuclear cells from human peripheral blood. Study of separated populations of mouse splenocytes and mononuclear cells from human peripheral blood showed that the TSST 1-induced proliferative response resided solely in the T cell populations.