Hengel H, Wagner H, Heeg K
Department of Medical Microbiology and Immunology, University of Ulm Albert-Einstein-Allee 11, Germany.
J Immunol. 1991 Aug 15;147(4):1115-20.
The requirement for protein kinase C (PKC) during triggering of murine CD8+ CTL was investigated. To this, CTL were depleted for PKC by pretreatment with PMA. This procedure neither influenced alpha/beta-TCR, CD3-epsilon, CD8, CD2, and lymphocyte function-associated Ag-1 expression, nor CTL-target cell conjugate formation. Although cytolytic effector function of PKC-depleted CTL triggered via alpha/beta-TCR structures was completely inhibited, target cell lysis induced via CD3-epsilon remained unaffected. Furthermore this PKC-independent cytolysis pathway was not associated with the release of serine esterases. Analyses at the clonal level revealed that PKC depletion blocked the cytolytic response of up to 95% of alpha/beta-TCR triggered CTL clones. The data suggest the existence of a distinct signaling pathway triggered via CD3-epsilon that is not associated with exocytosis of serine esterases and probably independent of PKC.
研究了在小鼠CD8⁺CTL触发过程中对蛋白激酶C（PKC）的需求。为此，通过用佛波酯（PMA）预处理使CTL中的PKC耗竭。该过程既不影响α/β-TCR、CD3-ε、CD8、CD2和淋巴细胞功能相关抗原-1的表达，也不影响CTL-靶细胞共轭体的形成。尽管通过α/β-TCR结构触发的PKC耗竭的CTL的细胞溶解效应功能被完全抑制，但通过CD3-ε诱导的靶细胞裂解不受影响。此外，这种不依赖PKC的细胞溶解途径与丝氨酸酯酶的释放无关。克隆水平的分析表明，PKC耗竭可阻断高达95%的α/β-TCR触发的CTL克隆的细胞溶解反应。数据表明存在一条通过CD3-ε触发的独特信号通路，该通路与丝氨酸酯酶的胞吐作用无关，可能也独立于PKC。
