Khanna M, Chaturvedi U C, Dhawan R, Tekwani B L, Pandey V C
Postgraduate Department of Microbiology, K.G. Medical College, Lucknow, India.
Immunology. 1991 Jan;72(1):73-8.
The present study was undertaken to investigate the role of calcium ions (Ca2+) in the cytotoxic activity of the cytotoxic factor (CF) produced by T lymphocytes of the dengue type 2 virus (DV)-infected mouse spleen. It was observed that CF prepared in Ca2(+)-free medium had no cytotoxic activity on normal mouse spleen cells suspended in Ca2(+)-free medium but had activity on cells suspended in medium having Ca2+. The cytotoxic activity of CF was restored by substitution with calcium chloride, the optimal dose being 10(-7) M. CF induced influx of Ca2+ as measured by uptake of radiolabelled calcium chloride (45Ca), in the susceptible target cells, macrophages (M phi) and T lymphocytes, but had no effect on CF-resistant B lymphocytes. Calcium channel blocking drugs, like verapamil, nifedipine and diltiazem, inhibited the cytotoxic activity of CF and also the CF-induced influx of 45Ca in M phi and T cells. Thus, presence of Ca2+ is obligatory for the cytotoxic activity of CF and the cell death is associated with increased intracellular Ca2+.
本研究旨在探讨钙离子(Ca2+)在登革2型病毒(DV)感染小鼠脾脏的T淋巴细胞产生的细胞毒性因子(CF)的细胞毒性活性中的作用。观察到在无Ca2+培养基中制备的CF对悬浮于无Ca2+培养基中的正常小鼠脾脏细胞无细胞毒性活性,但对悬浮于含Ca2+培养基中的细胞有活性。用氯化钙替代可恢复CF的细胞毒性活性,最佳剂量为10(-7)M。通过放射性标记氯化钙(45Ca)摄取测定,CF诱导易感靶细胞巨噬细胞(M phi)和T淋巴细胞中Ca2+内流,但对CF抗性B淋巴细胞无影响。钙通道阻滞剂,如维拉帕米、硝苯地平和地尔硫卓,抑制CF的细胞毒性活性以及CF诱导的M phi和T细胞中45Ca内流。因此,Ca2+的存在是CF细胞毒性活性所必需的,细胞死亡与细胞内Ca2+增加有关。