Cannon M J, Bangham C R
Division of Immunology, National Institute for Medical Research, Mill Hill, London, U.K.
J Gen Virol. 1989 Jan;70 ( Pt 1):79-87. doi: 10.1099/0022-1317-70-1-79.
Two mouse cytotoxic T cell (Tc) clones, D5 and H11a, with specificity for the respiratory syncytial virus (RSV) fusion protein (F) were derived from BALB/c mice primed intranasally (i.n.) with RSV (A2 strain). These clones possessed essentially the same characteristics, and only clone H11a is described here. Tc clone H11a lysed target cells infected with a recombinant vaccinia virus (VV) expressing the RSV F gene, and similar target cells infected with RSV strains Long, 8/60, or 18537. In addition, two RSV-specific mouse Tc lines are described, from BALB/c mice primed i.n. with RSV A2 (Tc line MJC-A2), or intraperitoneally with a VV-RSV F gene recombinant (Tc line MJC-F). Tc line MJC-A2 was of unknown antigen specificity, failing to lyse targets infected with recombinant VVs expressing the RSV nucleoprotein (N), large glycoprotein, F, 1A, 1C, or partial matrix protein (amino acid residues 88 to 257) genes. MJC-A2 Tc were cross-reactive for all strains of RSV tested. In contrast, the F-specific MJC-F Tc showed a marked degree of RSV strain specificity, efficiently lysing targets infected with RSV Long or A2 strains, but showing greatly reduced lysis of targets infected with RSV 8/60 or 18537 strains. An anti-RSV human Tc line, IH.K2, also recognized the fusion protein. IH.K2 Tc efficiently lysed autologous Epstein-Barr virus-transformed B cells (BCL) persistently infected with RSV A2 and BCL infected with a VV-RSV F gene recombinant. IH.K2 function was not exclusively RSV F-specific, however, as these cells also lysed autologous BCL infected with a VV-RSV N gene recombinant. These data show that the RSV fusion protein is a target antigen for anti-RSV Tc following infection of mice and humans, and that the F-specific Tc repertoire in mice can be influenced by the method and route of priming.
从经鼻内（i.n.）接种呼吸道合胞病毒（RSV，A2株）致敏的BALB/c小鼠中获得了两个对呼吸道合胞病毒融合蛋白（F）具有特异性的小鼠细胞毒性T细胞（Tc）克隆，即D5和H11a。这些克隆具有基本相同的特性，本文仅描述克隆H11a。Tc克隆H11a可裂解感染表达RSV F基因的重组痘苗病毒（VV）的靶细胞，以及感染RSV毒株Long、8/60或18537的类似靶细胞。此外，还描述了两个RSV特异性小鼠Tc系，一个来自经鼻内接种RSV A2致敏的BALB/c小鼠（Tc系MJC-A2），另一个来自经腹腔接种VV-RSV F基因重组体致敏的BALB/c小鼠（Tc系MJC-F）。Tc系MJC-A2的抗原特异性未知，它不能裂解感染表达RSV核蛋白（N）、大糖蛋白、F、1A、1C或部分基质蛋白（氨基酸残基88至257）基因的重组VV的靶细胞。MJC-A2 Tc对所有测试的RSV毒株具有交叉反应性。相比之下，F特异性的MJC-F Tc表现出明显程度的RSV毒株特异性，能有效裂解感染RSV Long或A2毒株的靶细胞，但对感染RSV 8/60或18537毒株的靶细胞的裂解能力大大降低。一个抗RSV人Tc系IH.K2也识别融合蛋白。IH.K2 Tc能有效裂解持续感染RSV A2的自体爱泼斯坦-巴尔病毒转化的B细胞（BCL）以及感染VV-RSV F基因重组体的BCL。然而，IH.K2的功能并非完全RSV F特异性，因为这些细胞也能裂解感染VV-RSV N基因重组体的自体BCL。这些数据表明，RSV融合蛋白是小鼠和人类感染后抗RSV Tc的靶抗原，并且小鼠中F特异性Tc库可受致敏方法和途径的影响。
