Complement-dependent, polymorphonuclear neutrophil-mediated cytotoxicity of herpesvirus-infected cells: possible mechanism(s) of cytotoxicity.
Highly enriched bovine polymorphonuclear neutrophils (PMN) were able to destroy herpesvirus-infected cells in the presence of complement. Our results suggest that some viral antigens are capable of activating the alternate complement pathway directly which results in cytotoxicity however, the addition of PMN plus complement resulted in high levels of cytotoxicity. Chelation of Ca2+ or Mg2+ indicated that Ca2+ was involved in PMN--target cell interactions but Mg2+ was involved in activation of the alternate complement pathway. Cytotoxicity in the presence of PMNs was shown to be under bidirectional control of cyclic nucleotides. Thus agents that elevated cAMP reduced cytotoxicity whereas agents that elevated GMP increased it. If the PMN is secreting some product during the cytotoxic reaction it must be performed since chemical shown to inhibit DNA, RNA and protein synthesis had no influence on CDNC. Our results are discussed in terms of the mechanism of CDNC lysis as well as in the vivo significance of such a defence mechanism.
D000818:Animals; D002118:Calcium / Q000276:immunology; D002417:Cattle; D002478:Cells, Cultured; D003170:Complement Pathway, Alternative; D003165:Complement System Proteins / Q000276:immunology; D003599:Cytoskeleton / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D005260:Female; D007241:Infectious Bovine Rhinotracheitis / Q000276:immunology*; D007372:Interferons / Q000276:immunology; D008274:Magnesium / Q000276:immunology; D008870:Microtubules / Q000276:immunology; D009504:Neutrophils / Q000276:immunology*; D009712:Nucleotides, Cyclic / Q000276:immunology
D009712:Nucleotides, Cyclic; D003165:Complement System Proteins; D007372:Interferons; D008274:Magnesium; D002118:Calcium