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观察卡介苗来源的热休克蛋白HSP65对小鼠移植黑色素瘤的抑制作用并初步探讨可能的作用机制。通过基因工程手段获得纯化的重组HSP65蛋白,与弗氏佐剂联合给药C57BL/6J小鼠。分别设计了两组免疫方案,一组于肿瘤细胞接种前免疫3次,另一组于肿瘤细胞接种前免疫7次。结果在免疫3次的情况下,虽然也能激发较高的特异性抗HSP65抗体,但抑瘤效果不明显(抑瘤率14.2%);增加免疫次数到7次后,抑瘤率高达73.2%,效果显著。经肿瘤组织病理切片发现,增加免疫次数导致肿瘤组织中灶性坏死增加,淋巴细胞浸润增加,且肿瘤细胞病理性核分裂相减少,提示了该疫苗作用的可能机制。
To observe the inhibitory effect of BCG-derived heat shock protein HSP65 on mouse melanoma and to explore its possible mechanism. Purified recombinant HSP65 protein was obtained by genetic engineering and C57BL / 6J mice were administered with Freund’s adjuvant. Two groups of immunization programs were designed respectively. One group was immunized three times before tumor cell inoculation and the other group was immunized seven times before tumor cell inoculation. Results In the case of 3 times of immunization, the anti-tumor effect was not obvious although the anti-HSP65 antibody was also stimulated with higher specificity (inhibition rate was 14.2%). After the number of immunizations was increased to 7 times, the anti-tumor rate was as high as 73.2% , The effect is remarkable. The pathological sections of tumor tissue showed that increasing the frequency of immunization resulted in the increase of focal necrosis and the increase of lymphocyte infiltration in tumor tissues, and the decrease of pathological mitosis of tumor cells, suggesting a possible mechanism of the vaccine.