Alcover A, Alberini C, Acuto O, Clayton L K, Transy C, Spagnoli G C, Moingeon P, Lopez P, Reinherz E L
Laboratory of Immunobiology, Dana-Farber Cancer Institute, Boston, MA.
EMBO J. 1988 Jul;7(7):1973-7. doi: 10.1002/j.1460-2075.1988.tb03035.x.
Human T lymphocytes can be activated through either the antigen/MHC receptor complex T3-Ti (CD3-Ti) or the T11 (CD2) molecule to proliferate via an IL-2 dependent mechanism. To investigate the relationship of these pathways to one another, we generated and characterized Jurkat mutants which selectively express either surface CD3-Ti or CD2. Here we show that CD3-Ti- mutants fail to be stimulated by either pathway to increase phosphoinositide turnover, mobilize calcium or induce the IL-2 gene. The activation capacity of these mutants via CD2 as well as CD3-Ti can be restored following reconstitution of surface CD3-Ti expression upon appropriate DNA transfer (e.g. Ti beta subunit cDNA into Ti beta- Jurkat variants). Collectively, these results demonstrate that CD3-Ti and CD2 pathways are interdependent and that phosphoinositide turnover is linked to the CD3-Ti complex.
人类T淋巴细胞可通过抗原/MHC受体复合物T3-Ti（CD3-Ti）或T11（CD2）分子被激活，进而通过白细胞介素-2依赖机制进行增殖。为了研究这些途径之间的相互关系，我们构建并鉴定了选择性表达表面CD3-Ti或CD2的Jurkat突变体。在此我们表明，CD3-Ti突变体无法被任何一条途径刺激来增加磷酸肌醇代谢、动员钙离子或诱导白细胞介素-2基因。在适当的DNA转移（如将Tiβ亚基cDNA导入Tiβ- Jurkat变体）后，表面CD3-Ti表达得以重建，这些突变体通过CD2以及CD3-Ti的激活能力也得以恢复。总体而言，这些结果表明CD3-Ti和CD2途径相互依赖，且磷酸肌醇代谢与CD3-Ti复合物相关联。
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