Biddison W E, Snodgrass H R, Bennink J, Effros R B, Doherty P C
J Exp Med. 1977 Aug 1;146(2):617-22. doi: 10.1084/jem.146.2.617.
Cytotoxic thymus-derived lymphocytes generated after interaction with trinitrophenyl (TNP)-substituted or virus-infected cells only lyse H-2 compatible target cells modified with the component used to immunize (TNP or virus). Prior saturation of TNP-reactive sites inhibits neither the infectivity of influenza A viruses, nor the capacity of infected cells to develop antigenic changes recognized by influenza-immune T cells. The two antigens are distinct entities on the cell membrane and do not obviously compete to form interactions with H-2 molecules.
与三硝基苯基(TNP)取代的或病毒感染的细胞相互作用后产生的细胞毒性胸腺来源淋巴细胞,仅裂解用用于免疫的成分(TNP或病毒)修饰的H-2相容靶细胞。TNP反应位点的预先饱和既不抑制甲型流感病毒的感染性,也不抑制感染细胞产生被流感免疫T细胞识别的抗原变化的能力。这两种抗原是细胞膜上的不同实体,不会明显竞争与H-2分子形成相互作用。