Ida H, Robertson M J, Voss S, Ritz J, Anderson P
Division of Tumor Immunology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
J Immunol. 1997 Sep 1;159(5):2154-60.
CD94 (Kp43) is a member of the human C-type lectin superfamily encoding type II membrane glycoproteins expressed on NK cells and a subset of T cells. Ligation of CD94 has been shown to either potentiate or inhibit NK cell proliferation and cytolytic effector function. Here we show that CD94 ligation triggers apoptosis in IL-2-primed NK cells. Evidence for CD94-induced apoptosis includes: 1) chromatin condensation as measured by increased fluorescence of Hoechst dye, 2) induction of DNA fragmentation, and 3) characteristic morphology by transmission electron microscopy. IL-2 priming (at least 12 h) is required for activation-induced NK cell death triggered by CD94. Activation-induced NK cell death triggered by CD94 ligation is extremely rapid (DNA fragmentation is first observed at 120 min). Unlike activation-induced T cell death, it is not inhibited by neutralizing Abs reactive with TNF-alpha or Fas ligand. Our results suggest that CD94 may play a role in the elimination of activated NK cells during the transition from the innate to the Ag-specific immune response.
CD94（Kp43）是人类C型凝集素超家族的成员，编码在自然杀伤（NK）细胞和一部分T细胞上表达的II型膜糖蛋白。已证明CD94的连接可增强或抑制NK细胞增殖和细胞溶解效应功能。在此我们表明，CD94连接可触发白细胞介素-2（IL-2）预刺激的NK细胞凋亡。CD94诱导凋亡的证据包括：1）通过Hoechst染料荧光增强测定的染色质浓缩，2）DNA片段化的诱导，以及3）透射电子显微镜观察到的特征性形态。IL-2预刺激（至少12小时）是CD94触发的激活诱导的NK细胞死亡所必需的。CD94连接触发的激活诱导的NK细胞死亡极其迅速（在120分钟时首次观察到DNA片段化）。与激活诱导的T细胞死亡不同，它不受与肿瘤坏死因子-α（TNF-α）或Fas配体反应的中和抗体抑制。我们的结果表明，CD94可能在从先天免疫反应向抗原特异性免疫反应转变过程中活化NK细胞的清除中发挥作用。
