【摘要】 目的研究热休克蛋白65 B细胞表位经皮下免疫高脂膳食动物对动脉粥样硬化(As)斑块生成的影响。方法利用HSP65上与炎症性自身免疫性疾病相关的两段功能表位P1(179-190)、P2(31-46),以CTB为载体蛋白构建高效表达载体p ET28a-CTB-p117,提取纯化获得可用于动物实验的蛋白,皮下免疫新西兰大白兔,比较抗HSP65抗体、血液总胆固醇含量变化与主动脉粥样硬化斑块的生成情况。结果能够诱导产生抗HSP65的抗体,血液中总胆固醇含量与对照组比较显著提高,并且能显著增加主动脉As斑块生成(P<0.05)。结论 HSP65相关表位蛋白以CTB为载体蛋白,在弗氏不完全佐剂条件下,经皮下免疫能显著加重As斑块生成,分析是因为抗HSP65抗体生成,促进炎症反应,脂类代谢变化进而促进As斑块的形成。可基于此,利用以上表位,改变免疫方式,设计出可用于降低斑块生成的抑制As斑块生成的免疫调节剂。对于CTB单独皮下免疫也致As斑块加重的结果需进一步实验考察验证。更多还原

【Abstract】 Aim To study the immunization effects of B epitopes of heat shock protein 65 on the atherosclerosis plaque formation of high fat diets animals. Methods By using two functional epitopes P1( 179-190),P2( 31-46) of HSP65 related to inflammatory autoimmune disease,high-level expression vector of p ET28a-CTB-p117 was built with CTB as a carrier protein. The fusion protein of CTB-p117 was acquired by expression and purification process and used to immunize the animals by subcutaneous and intracutaneous injections. Results Anti-HSP65 antibodies were induced and both blood total cholesterol levels and aortic As plaques significantly increased compared with control group( P < 0. 05).Conclusions The HSP65 epitopes( CTB as the carrier protein) were able to aggravate As plaque formation after subcutaneous injections which could be the reasons that the induced anti-HSP65 antibodies promoted inflammatory reaction,lipid metabolic changes,and then accelerate the As plaque formation. The above HSP65 epitopes can be used to construct the anti-As vaccine to inhibit the As plaque formation by different immunization way.更多还原