Cell-mediated cytotoxicity against sendai-virus-infected cells

Abstract

After injection of Sendai virus, a parainfluenza virus type 1, mice generate cytotoxic lymphocytes which lyse specifically Sendai-virus-infected target cells in vitro. Their action is not inhibited by specific antibody in vitro. Killer cell activity appears 4 days after infection, reaches a maximum on the 7th day and disappears on the 14th to 16th day. Decrease of cytotoxic cell activity is correlated with an increase of haemagglutinating antibodies. The cytotoxic effector cell could be characterized as a thymus-derived cell, there is no specific activity in antibody-dependent cell-mediated cytolysis (ADCC). The degree of cytotoxic effector cell activity is only slightly influenced by the dose of injected infective virus. *) This work was supported by the Deutsche Forschungsgemeinschaft. Cell-Mediated Cytotoxicity against Sendai-Virus-infected Cells • 129 Using different syngeneic Sendai-virus-infected cells as targets for cell-mediated cytotoxicity, a tumor line was not lysed by cytotoxic lymphocytes in spite of viral surface antigens. Preliminary experiments were performed to demonstrate the H-2 gene restriction of the cytotoxic interaction. Using macrophages and tumor cells as targets only syngeneic infected target cells were lysed.

Cytotoxic Interactions of Virus Specific Effector Cells With Virus Infected Targets of Different Cell Type*

“…Cell mediated specific lysis of targets modified by viral infections (Zinkernagel I % Doherty, 1974;Gardner et af., 1975;Koszinowski & Thomssen, 1975;Ertl & Koszinowski, 1976), tumour antigens (Schrader & Edelman, 1976), chemical agents (Shearer, 1974), the male histocompatibility antigen of the mouse (Gordon et al, 1975) and minor histocompatibility antigens (Bevan, 1975) is restricted to K or D compatibility between target and effector cell. Data presented here show the same restrictions in the Sendai virus infection when primary cells were used as targets.…”

Cell-mediated immunity induced in mice after vaccination with a protease activation mutant, TR-2, of Sendai virus

“…In Sendai virus-specific CTL, coincidence in the H-2K region seems important rather than that in the H-2D region (13,25,34,35,39,41,59). Several reports demonstrated that inbred mice of the H-2k haplotype were low responders to secondary in vitro stimulation of CTL (14,40,53), whereas other investigations showed that H-2k mice generated normal CTL responses (5,7,16,24,37,39,61). The present data indicated that CTL could be elicited in H-2k-bearing C3H/He mice by intranasal infection with TR-2 and a secondary CTL response could be stimulated in vivo by reinfection with wild-type Sendai virus.…”