Shirai M, Chen M, Arichi T, Masaki T, Nishioka M, Newman M, Nakazawa T, Feinstone S M, Berzofsky J A
Department of Microbiology, Yamaguchi University School of Medicine, Japan.
J Infect Dis. 1996 Jan;173(1):24-31. doi: 10.1093/infdis/173.1.24.
The induction of virus-specific cytotoxic T lymphocytes (CTL) is an important part of vaccine strategy. CTL induction in vivo by two hepatitis C virus (HCV) peptides containing CTL epitopes, one from the NS5 region (P17) and one from the core (C7), was compared. P17 required covalent attachment of a helper peptide (PCLUS3 containing a cluster of epitopes from the human immunodeficiency virus envelope protein), whereas C7 did not. However, the minimal decapeptide of C7, C7A10, alone did not induce CTL. The helper cells induced by PCLUS3-17 or by C7 were shown to be CD4+ and to produce interleukin-2 (IL-2). Thus, help can be supplied by a natural helper epitope intrinsic to the CTL peptide, as in C7, or by attaching a helper epitope from another protein, as in the case of P17. The cluster peptides may be useful promiscuous helper peptides for a variety of CTL epitopes from diverse pathogens.
诱导病毒特异性细胞毒性T淋巴细胞（CTL）是疫苗策略的重要组成部分。比较了两种含有CTL表位的丙型肝炎病毒（HCV）肽在体内诱导CTL的情况，一种来自NS5区（P17），另一种来自核心区（C7）。P17需要与一种辅助肽（PCLUS3，含有来自人类免疫缺陷病毒包膜蛋白的一组表位）共价连接，而C7则不需要。然而，单独的C7最小十肽C7A10并不能诱导CTL。由PCLUS3-17或C7诱导的辅助细胞显示为CD4+并产生白细胞介素-2（IL-2）。因此，辅助作用可以由CTL肽固有的天然辅助表位提供，如C7的情况，也可以通过连接来自另一种蛋白质的辅助表位来提供，如P17的情况。这些簇肽可能是用于来自不同病原体的多种CTL表位的有用通用辅助肽。
