Shatrova A N, Zenin V V, Aksenov N D, Mitiushova E V, Marakhova I I
Tsitologiia. 2011;53(8):652-8.
The expression of alpha-subunit of interleukin-2 receptor (IL-2Ralpha) was assessed by quantifying activation-induced upregulation of CD25 in human blood lymphocytes (HBL) stimulated by interleukin-2 (IL-2). It was established that exogenous IL-2 induced no surface expression of CD25 neither proliferation at 48 h of IL-2 action. In component HBL, pretreated by sub-mitogenic doses of phytohemagglutinin (PHA), 5-15 % of cell population was revealed to represent the CD2t+ cells, and in the competent cells only, exogenous IL-2 induced the surface expression of CD25 as well as the growth and the proliferative response, which was comparable with those to mitogenic doses of PHA. The JAK3 inhibitor WHI-P131 eliminated IL-2-dependent CD25 expression without influencing the CD25 expression in competent cells. Unlike, PP2 was found to inhibit the IL-2-dependent CD25 expression in a lesser extent than WHI-P131, however this drug was effectively inhibited CD25 expression in PHA-pretreated, competent HBL. These data suggest that Src-dependent signaling participate in the early IL-2Ralpha expression that precedes the IL-2-dependent cell cycle progression of activated HBL. It is concluded that in normal T cells, the IL-2Ralpha expression in firstly induced by antigen (mitogen) and thereafter it is held IL-2 through JAK-dependent signaling pathway.
通过量化白细胞介素-2（IL-2）刺激的人血淋巴细胞（HBL）中活化诱导的CD25上调来评估白细胞介素-2受体（IL-2Rα）α亚基的表达。结果表明，外源性IL-2在作用48小时时既未诱导CD25的表面表达，也未诱导增殖。在经亚致有丝分裂剂量的植物血凝素（PHA）预处理的HBL组分中，发现5-15%的细胞群体为CD2t+细胞，并且仅在有反应能力的细胞中，外源性IL-2诱导了CD25的表面表达以及生长和增殖反应，这与对致有丝分裂剂量PHA的反应相当。JAK3抑制剂WHI-P131消除了IL-2依赖性CD25表达，而不影响有反应能力细胞中的CD25表达。与之不同的是，发现PP2对IL-2依赖性CD25表达的抑制程度小于WHI-P131，然而该药物有效地抑制了PHA预处理的有反应能力的HBL中的CD25表达。这些数据表明，Src依赖性信号传导参与了活化的HBL的IL-2依赖性细胞周期进展之前的早期IL-2Rα表达。得出的结论是，在正常T细胞中，IL-2Rα表达首先由抗原（有丝分裂原）诱导，然后通过JAK依赖性信号通路由IL-2维持。
