Alli Rajshekhar, Savithri Balasubramanian, Das Suvendu, Varalakshmi Chavvakula, Rangaraj Nandini, Khar Ashok
Centre for Cellular and Molecular Biology, Hyderabad, India.
Eur J Immunol. 2004 Apr;34(4):1119-26. doi: 10.1002/eji.200324793.
DC are the most efficient antigen-presenting cells that regulate the immune response. Here, we demonstrate the expression of NK cell receptor protein-2 (NKR-P2) on rat and mouse DC, and we show that NKR-P2 gets reorganized upon antigen contact. DC activated with anti-NKR-P2 mAb exhibit enhanced apoptotic killing of tumor targets, whereas blocking the interaction between NKR-P2 and its ligand with rNKR-P2 abrogated apoptotic killing, suggesting NKR-P2 to function as an activating molecule on DC. In vivo injection of anti-NKR-P2 mAb augmented DC activity and delayed tumor progression. NKR-P2 signaling involved Ca(2+ )influx, culminating in the expression of the apoptosis-inducing molecule, TNF-alpha. Taken together, these observations suggest that NKR-P2 (the rat orthologue of human NKG2D) acts as a target-recognition molecule on DC.
树突状细胞（DC）是调节免疫反应的最有效的抗原呈递细胞。在此，我们证明了NK细胞受体蛋白2（NKR-P2）在大鼠和小鼠DC上的表达，并且我们表明NKR-P2在抗原接触后会重新组织。用抗NKR-P2单克隆抗体激活的DC对肿瘤靶标的凋亡杀伤增强，而用重组NKR-P2阻断NKR-P2与其配体之间的相互作用则消除了凋亡杀伤，这表明NKR-P2在DC上作为激活分子发挥作用。体内注射抗NKR-P2单克隆抗体增强了DC活性并延缓了肿瘤进展。NKR-P2信号传导涉及Ca(2+)内流，最终导致凋亡诱导分子TNF-α的表达。综上所述，这些观察结果表明NKR-P2（人类NKG2D的大鼠同源物）在DC上作为靶标识别分子发挥作用。
