Tchilian E Z, Anderson G, Moore N C, Owen J J, Jenkinson E J
Department of Anatomy/Centre for Clinical Research in Immunology and Signalling, University of Birmingham, UK.
Immunology. 1996 Apr;87(4):566-72. doi: 10.1046/j.1365-2567.1996.515580.x.
Ligation of T-cell receptor (TCR) causes mature T cells to proliferate or, on re-exposure to antigen, can cause them to die by activation-induced cell death (AICD). In proliferative responses, costimulatory and adhesive interactions are required and activation of protein kinase C (PKC) has been shown to be essential. Whether or not interactions involving costimulatory signals and PKC have a role in facilitating AICD remains unclear. Here we have examined the role of CD28/B7 and leucocyte function associated antigen-1 (LFA-1)/intracellular adhesion molecule (ICAM) mediated interactions in AICD triggered by staphylococcal enterotoxin B (SEB) in murine lymph node T cells. We show that, after a primary proliferative response to SEB, LFA-1/ICAM-2 adhesive interactions can play a part in AICD following SEB rechallenge, while B7 and ICAM-1 mediated interactions are not essential for this process. In addition, using a highly selective PKC inhibitor, Ro31.8425, we show that PKC activation is essential for the regulation of AICD by SEB rechallenge.
T细胞受体（TCR）的结扎会导致成熟T细胞增殖，或者在再次接触抗原时，可通过活化诱导的细胞死亡（AICD）导致它们死亡。在增殖反应中，需要共刺激和黏附相互作用，并且蛋白激酶C（PKC）的激活已被证明是必不可少的。涉及共刺激信号和PKC的相互作用是否在促进AICD中起作用仍不清楚。在这里，我们研究了CD28/B7和白细胞功能相关抗原-1（LFA-1）/细胞间黏附分子（ICAM）介导的相互作用在鼠淋巴结T细胞中由葡萄球菌肠毒素B（SEB）触发的AICD中的作用。我们表明，在对SEB的初次增殖反应后，LFA-1/ICAM-2黏附相互作用可在SEB再次攻击后的AICD中起作用，而B7和ICAM-1介导的相互作用对该过程不是必需的。此外，使用高度选择性的PKC抑制剂Ro31.8425，我们表明PKC激活对于SEB再次攻击对AICD的调节至关重要。
