Cytochalasins enhance the proliferation of CD4 cells through the CD3-Ti antigen receptor complex or the CD2 molecule through an effect on early events of activation.
Cytochalasins enhance the proliferation of CD4 cells through the CD3-Ti antigen receptor complex or the CD2 molecule through an effect on early events of activation.
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细胞松弛素通过 CD3-Ti 抗原受体复合物或 CD2 分子通过影响早期激活事件来增强 CD4 细胞的增殖。
DOI：
10.4049/jimmunol.146.11.3736
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发表时间：
1991
影响因子：
4.4
通讯作者：
T. Abe
中科院分区：
文献类型：
--
作者：
T. Matsuyama;A. Yamada;K. Deusch;J. Sleasman;J. Daley;Y. Torimoto;T. Abe
已知细胞松弛素以浓度依赖性方式抑制或增强由有丝分裂原诱导的T细胞增殖。为了阐明细胞松弛素增强T细胞增殖的机制，我们研究了细胞松弛素影响信号转导中的激活途径和事件。我们还研究了CD 4细胞亚群对细胞松弛素的优先反应。细胞松弛素可促进最适剂量抗CD 3抗体或次适剂量抗CD 2抗体诱导的CD 4细胞增殖。细胞松弛素，在低浓度下，增强了细胞内Ca 2+的上升和生产的IP 3在CD 4细胞激活的抗CD 2或CD 3抗体。细胞松弛素也能增强抗CD 3抗体对CD 3的调节作用。这些结果表明，细胞松弛素增强CD 4细胞的增殖，通过影响早期事件的信号转导后，通过CD 3-Ti Ag受体复合物或CD 2分子激活。在使用的剂量下，细胞松弛素似乎与细胞膜中的细胞松弛素结合位点相互作用。细胞松弛素主要增强CD 4细胞的CD 29亚群中的CD 3介导的增殖。
Cytochalasins are known to inhibit or enhance the proliferation of T cells induced by mitogens in a concentration-dependent fashion. To clarify the mechanism by which cytochalasins enhance T cell proliferation, we examined which activation pathways and events in signal transduction were affected by cytochalasins. We also examined subsets of CD4 cells for a preferential response to cytochalasins. Cytochalasins enhanced the proliferation of CD4 cells induced by optimal doses of anti-CD3 antibody or suboptimal doses of anti-CD2 antibodies. Cytochalasins, at low concentrations, enhanced the rise in intracellular Ca2+ and production of IP3 in CD4 cells activated by anti-CD2 or CD3 antibodies. Cytochalasins also enhanced the modulation of CD3 induced by anti-CD3 antibody. These results suggest that cytochalasins enhance the proliferation of CD4 cells by affecting early events in signal transduction after activation through the CD3-Ti Ag-receptor complex or CD2 molecule. At the doses used, cytochalasins appear to interact with cytochalasin-binding sites in the cell membrane. Cytochalasins predominantly enhanced CD3-mediated proliferation in the CD29-subset of CD4 cells.