Protease inhibition of natural killer (NK) and antibody-dependent cell-mediated cytoxicity (ADCC) activities

J Lab Clin Med. 1984 Feb;103(2):215-22.

Abstract

The ability of protease inhibitors to modulate NK and ADCC cell activities was studied. NK and ADCC cell activities were suppressed by 1,10 phenanthroline (PHE), N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK), L-1-tosylamide-2-phenylethylchoromethyl ketone (TPCK), N-benzoyl-DL-tyrosine ethyl ester (BTEE), and phenylethylchoromethyl fluoride (PMSF). The effect of these protease inhibitors on ADCC was not mediated through the early phase of cytotoxicity involving Fc-receptor binding, since they failed to alter EoxA rosetting of effector cells. The results suggest that an activated esterase system might play a role in the later phase of the cytotoxic mechanism by ADCC cells and perhaps NK cells.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Antibody-Dependent Cell Cytotoxicity / drug effects*
  • Dimethyl Sulfoxide / pharmacology
  • Ethanol / pharmacology
  • Female
  • Humans
  • In Vitro Techniques
  • Killer Cells, Natural / drug effects*
  • Protease Inhibitors / pharmacology*
  • Rats
  • Rats, Inbred BUF
  • Receptors, Fc / drug effects
  • Receptors, Fc / metabolism
  • Rosette Formation
  • Spleen / drug effects

Substances

  • Protease Inhibitors
  • Receptors, Fc
  • Ethanol
  • Dimethyl Sulfoxide