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细菌性超抗原可作为主要组织相容性复合物(MHC)Ⅱ类分子的配体,又能与T细胞抗原受体β链可变区(TCR Vβ)结合。每一细菌性超抗原分别对一组TCR Vβ有其特定的亲和性,多克隆激活T细胞,可促使细胞因子病理性增高,继而引起毒性休克综合征等疾病。本文讨论了与MHCⅡ类分子或TCR结合作用减弱的细菌性起抗原,在保护实验动物免受野生到细菌性超抗原攻击的效果。作者采用基因工程方法,制备突变型金黄色葡萄球菌肠毒素A (MTSEA):将64、92位上酪氨酸置换成丙氨酸。将SEA与佐剂混合后,分别以2μg或10μg野生型SEA(WT-SEA)或MTSEA注入C57BL/6 /小鼠腹腔,另以单独注射佐剂的小鼠作为对照,2～4周
Bacterial superantigens can be used as ligands for the major histocompatibility complex (MHC) class II molecules and for binding to the TCR Vβ domain. Each bacterial superantigen has a specific affinity for a group of TCR Vβ, polyclonal activation of T cells, can promote the pathological increase of cytokines, which in turn cause toxic shock syndrome and other diseases. This article discusses the effect of bacterial antigens with reduced binding to MHC class II molecules or TCRs in the protection of experimental animals from wild-to-bacterial superantigens. The authors used a genetic engineering method to prepare mutant S. aureus enterotoxin A (MTSEA): replacing tyrosine at positions 64 and 92 with alanine. After SEA was mixed with adjuvant, C57BL / 6 / mice were injected intraperitoneally with 2μg or 10μg of wild-type SEA (WT-SEA) or MTSEA respectively and the mice injected with adjuvant alone were given as control.