Purified human T cells stimulated with cross-linked anti-CD3 monoclonal antibody OKT3: rIL-1 is a co-stimulatory factor for CD4+CD29+CD45RA- T cells.
Purified human T cells stimulated with cross-linked anti-CD3 monoclonal antibody OKT3: rIL-1 is a co-stimulatory factor for CD4+CD29+CD45RA- T cells.
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用交联抗 CD3 单克隆抗体 OKT3 刺激的纯化人 T 细胞：rIL-1 是 CD4 CD29 CD45RA-T 细胞的共刺激因子。
DOI：
10.1111/j.1365-3083.1990.tb02930.x
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发表时间：
1990
影响因子：
3.7
通讯作者：
Bach,FH
中科院分区：
文献类型：
--
作者：
Panzer,S;Geller,RL;Bach,FH
辅助细胞(AC)被认为在T细胞激活中扮演两个主要角色：它们连接某些刺激，如单抗，它们提供所需的细胞因子。为了区分这些作用，我们用Fc特异性的山羊抗鼠免疫球蛋白包被的聚苯乙烯头将OKT3交联到高纯度的T细胞上，并研究了外源添加细胞因子后T细胞的激活。加入AC、rIL-2或rIL-1后，CD25表达上调，细胞增殖，细胞毒作用增强。在AC或rIL-2作用下，CD4+和CD8+细胞均被激活，而在rIL-1作用下，仅有CD4+CD29+CD4SRA细胞有反应。抗IL-2R P55(抗TAC)单抗可抑制rIL-2或rIL-1支持的增殖反应。抗TAC需要补充抗IL-6抗体，或加入10倍以上的浓度。含有AC的培养物产生的IL-2比添加rIL-1的培养物更多。只有含有AC的培养物也产生可检测到的量的IL-6。这些发现结合观察到，在六个独立的实验中，每个独立实验中统计的2000个纯化的T细胞都没有表达MHC II类抗原，这强烈表明rIL-I可以直接激活T细胞，而不是通过增强污染AC的功能来间接激活T细胞。
Accessory cells (AC) are believed to play two major roles in T‐cell activation: they cross‐link certain stimuli such as monoclonal antibodies, and they provide needed cytokines. To differentiate between these roles, we cross‐linked OKT3 on highly purified T‐cells by means of Fc‐specific goat anti‐mouse IgG‐coated polystyrene heads and studied T‐cell activation after exogenously added cytokines. Following addition of AC, rIL‐2. or rIL‐1. CD25 was up‐regulated, and the cells proliferated and became cytotoxic. Both CD4+and CD8+cells were activated in the presence of AC or rIL‐2. In contrast, only CD4+CD29+CD4SRA cells responded in the presence of rIL‐1. Anti‐IL‐2R p55 (anti‐TAC) monoclonal antibody inhibited the proliferative response supported by rIL‐2 or rIL‐1. To inhibit proliferation of cells stimulated in the presence of AC. anti‐TAC needed to be supplemented with anti‐IL‐6 antibodies, or to be added in a 10‐fold higher concentration. Cultures with AC produced larger amounts of IL‐2 than those supplemented with rIL‐1. Only AC‐containing cultures also produced detectable amounts of IL‐6. These findings combined with the observation that none of 2000 purified T cells counted in each of six independent experiments expressed MHC class II antigens strongly suggest that rIL‐I can activate T cells directly, rather than indirectly by potentiating the function of contaminating AC.