The acquisition of anti-influenza virus activity by macrophages.
Exposure of resident peritoneal macrophages or thioglycollate-induced macrophages (TG-Mø) to influenza or Sendai virus-infected spleen cell culture supernatants (MAS) resulted in macrophage activation. When normal resident macrophages were used as effector cells, both infected P815 and L929 cells were lysed in the presence of MAS. MAS-activated TG-Mø also lysed influenza virus-infected L929 cells. Histocompatibility between effector cells and target cells was not required for target cell destruction. The effector cells were plastic-adherent, phagocytic and Ia-. MAS-activated macrophages were also resistant to influenza virus infection in vitro. Both infectious and non-infectious preparations of influenza or Sendai virus preparations were effective at generating MAS. The mediator(s) which renders macrophages to become cytotoxic and resistant to infection was acid-stable, heat-labile (56 degrees C, 30 min; or 100 degrees C, 5 min), and the activity was neutralized by sheep antimouse type 1 interferon (IFN).
D000818:Animals; D003602:Cytotoxicity, Immunologic; D066298:In Vitro Techniques; D009980:Influenza A virus / Q000276:immunology*; D007370:Interferon Type I / Q000276:immunology; D007700:Kinetics; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D010222:Parainfluenza Virus 1, Human / Q000276:immunology*; D013154:Spleen / Q000276:immunology
D007370:Interferon Type I