摘要
动脉粥样硬化是一种自身免疫性疾病。人自身热休克蛋白60是主要的自身免疫原之一，能引起人自身免疫性反应进而促进动脉粥样硬化的发生，热休克蛋白65与人热休克蛋白60有较高的同源性，同源性为46％左右，具有相似的抗原表位，通过诱导粘膜免疫耐受产生抗炎效果将会对动脉粥样硬化产生积极的影响。热休克蛋白65鼻黏膜免疫动脉粥样硬化模型新西兰大白兔，能显著减轻主动脉粥样斑块，与PBS组存在极显著差异（P〈0．01）。热休克蛋白65上31-46片段，180-188片段与霍乱毒素B亚单位的融合蛋白鼻黏膜免疫动脉粥样硬化模型新西兰大白兔．不能显著减轻主动脉粥样斑块，与PBS组不存在显著性差异（P〉0．05）。结果表明HSP65鼻黏膜免疫新西兰大白兔能有效诱导兔黏膜免疫耐受，预防动脉粥样硬化；热休克蛋白65上31-46片段和180～188片段，虽然有文献报道通过诱导免疫耐受在小鼠自身免疫性疾病佐剂性关节炎中有很好的预防作用，但在动脉粥样硬化中却不能有效诱导黏膜免疫耐受而显著改善病情。
Atherosclerosis is an autoimmune disease. Human heat shock protein 60 is one of the major autoantigens, which can bring autoimmune reaction and lead to atherosclerosis. HSP60 and HSP65 are highly homologous, sharing several similar epitopes. Therefore, inducing immune tolerance to HSP65 could bring positive effect to atherosclerosis. Immunizing the New Zealand rabbits with HSP65 by nasal mueosa can transfer atherosclerosis, and this difference is utmostly notable between HSP65 group and PBS group（P〈0. 01）. Vaccinating the New Zealand rabbits with the fusion protein including the 31-46 peptide of HSP65, the 180-188 peptide of HSP65 and cholera toxin B subunit, can neither induce immune tolerance nor inhibit atherosclerosis. The results showed that immunizing the New Zealand rabbits with HSP65 intranasally can induce immune tolerance to HSP65 effectively and inhibit atherosclerosis, however, the 31-46 peptide and the 180-188 peptide of HSP65, which can inhibit adjuvant Arthritis, failed to induce immune tolerance to HSP65 in the New Zealand rabbits and showed no protection against atherosclerosis.
出处
《药物生物技术》
CAS
CSCD
2009年第1期1-7,共7页
Pharmaceutical Biotechnology
基金
国家自然科学基金资助项目(NO.30672464
No.30701023)
