Interaction between T cells and murine acquired immunodeficiency virus superantigen: effect of second signal on T cell reactivity to the MAIDS virus superantigen.
Interaction between T cells and murine acquired immunodeficiency virus superantigen: effect of second signal on T cell reactivity to the MAIDS virus superantigen.
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T 细胞与鼠获得性免疫缺陷病毒超抗原之间的相互作用：第二信号对 T 细胞对 MAIDS 病毒超抗原反应性的影响。
DOI：
10.1093/intimm/5.6.583
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发表时间：
1993
影响因子：
4.4
通讯作者：
Kanagawa,O
中科院分区：
文献类型：
--
作者：
Heise,M;Chow,K;Kanagawa,O
小鼠获得性免疫缺陷（MAIDS）病毒转化的B细胞系B6-1710显示出表达超抗原活性并刺激T细胞杂交瘤产生IL-2。然而，建立B6-1710反应性杂交瘤的T细胞克隆和系在用B6-1710刺激后不能增殖，而B6-1710细胞能够呈递细菌超抗原以刺激T细胞杂交瘤和克隆。T细胞对MAIDS病毒超抗原的免疫应答可以通过加入药理学试剂佛波醇肉豆蔻酸酯（PMA）来检测。因此，B6-1710似乎缺乏T细胞对MAIDS病毒超抗原的增殖反应所需的刺激活性。在幼稚脾T细胞对MAIDS超抗原的应答分析中，在PMA存在下，从用B6-1710细胞刺激的培养物中回收的T细胞未显示出优势TCR Vβ链使用，而从仅用B6-1710刺激的培养物中回收的细胞由表达Vβ5、11和12 TCR链的T细胞占优势。这些结果表明，携带大部分TCR Vβ链的T细胞能够对B6-1710超抗原产生应答。T细胞和病毒超抗原之间相互作用的亲合力在T细胞之间可能显著不同，并且那些表现出与MAIDS病毒超抗原弱相互作用的T细胞可能需要额外的信号，如PMA，用于对B6-1710细胞的体外增殖应答。
A murine acquired Immunodeficiency (MAIDS) virus transformed B cell line, B6-1710, was shown to express superantigen activity and stimulate T cell hybridomas to produce IL-2. However, T cell clones and lines from which B6-1710 reactive hybridomas were established failed to proliferate upon stimulation with B6-1710, while B6-1710 cells were capable of presenting bacterial superantigen to stimulate both T cell hybridomas and clones. Proliferative response of T cells to MAIDS virus superantigen could be detected by the addition of the pharmacological agent phorbol myristate acetate (PMA). Thus, B6-1710 seems to lack a stimulatory activity necessary for the prollferative response of T cells to the MAIDS viral superantigen. In the analysis of the response of naive splenic T cells to the MAIDS superantigen, T cells recovered from a culture stimulated with B6-1710 cells in the presence of PMA showed no dominant TCR Vβchain usage, while cells recovered from a culture stimulated with B6-1710 alone were dominated by T cells expressing Vβ5, 11, and 12 TCR chains. These results suggest that T cells bearing a majority of TCR Vβchains are capable of responding to B6-1710 superantigen. The avidity of interaction between T cells and viral superantigen may differ significantly among T cells and those T cells exhibiting weak interaction with MAIDS virus superantigen may require additional signals, such as PMA, for anin vitroproliferative response to B6-1710 cells.