Smialowicz R J, Rogers R R, Riddle M M, Luebke R W, Rowe D G, Garner R J
J Immunopharmacol. 1984;6(1-2):1-23. doi: 10.3109/08923978409026455.
Natural killer (NK) cell activity of mice given a single injection of manganese chloride (MnCl2) was significantly enhanced as measured in a 4-hr in vitro 51Cr release assay. Enhanced activity persisted for several days after injection. This cytotoxic activity was associated with nonadherent spleen cells and was completely eliminated by injecting MnCl2-treated mice with anti-asialo GM1 serum. Manganese-enhanced natural cytotoxicity was observed in several mouse strains with differing NK cell reactivity (CBA/J, C57BL/6, A/J, C3H/HeJ, and C57BL/6 beige mice) and with several tumor target cells with differing sensitivity to NK cytolysis (YAC-1, RBL-5, EL-4, and P815). The growth of B16-F10 melanoma lung tumors was inhibited in mice injected with MnCl2 one day before tumor challenge. Manganese chloride enhancement of NK cell activity appeared to be mediated by interferon (IFN). Low levels of IFN were detected in the serum of mice as early as 4 hr after MnCl2 injection. Rabbit anti-mouse IFN alpha, beta but not anti-mouse IFN gamma completely eliminated the MnCl2-enhanced NK cell activity in the spleens of mice. The observed enhancement of NK cell activity by MnCl2 is similar to that reported for more complex molecules that act by inducing IFN production.
在4小时的体外51Cr释放试验中，单次注射氯化锰（MnCl2）的小鼠的自然杀伤（NK）细胞活性显著增强。注射后，增强的活性持续了数天。这种细胞毒性活性与非贴壁脾细胞有关，并且通过给注射了MnCl2的小鼠注射抗唾液酸GM1血清可完全消除。在几种具有不同NK细胞反应性的小鼠品系（CBA/J、C57BL/6、A/J、C3H/HeJ和C57BL/6米色小鼠）以及几种对NK细胞溶解具有不同敏感性的肿瘤靶细胞（YAC-1、RBL-5、EL-4和P815）中均观察到锰增强的自然细胞毒性。在肿瘤攻击前一天注射MnCl2的小鼠中，B16-F10黑色素瘤肺肿瘤的生长受到抑制。氯化锰对NK细胞活性的增强似乎是由干扰素（IFN）介导的。早在注射MnCl2后4小时，就在小鼠血清中检测到低水平的IFN。兔抗小鼠IFNα、β而非抗小鼠IFNγ完全消除了小鼠脾脏中MnCl2增强的NK细胞活性。观察到的MnCl2对NK细胞活性的增强与报道的通过诱导IFN产生而起作用的更复杂分子的增强相似。
