Contrasting effects of RNA and protein synthesis blocking on natural and lectin-dependent cell-mediated cytotoxicity against adherent HEp-2 cells.
In this study, earlier observations concerning the independence of both natural (NCMC) and lectin-dependent cell-mediated cytotoxicity (LDCC) from DNA synthesis have been confirmed. In addition, blocking of RNA synthesis by actinomycin D and of protein synthesis, reversibly by puromycin (PM) and irreversibly by emetine (EM) had different effects on NCMC and LDCC against 3H-thymidine-prelabeled HEp-2 target cells. Similarly to the Con A-induced proliferation of lymphocytes, LDCC activity was also inhibited by blocking of RNA and protein synthesis. NCMC to HEp-2 target cells was not affected by blocking of RNA synthesis, while both PM and EM strongly enhanced NCMC activity.
A
A
Perl
R
R
Gonzalez-Cabello
L
L
Falucskai
P
P
Gergely
J
J
Fehér
D002448:Cell Adhesion; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival; D003208:Concanavalin A / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004640:Emetine / Q000494:pharmacology; D006801:Humans; D007111:Immunity, Cellular; D037102:Lectins / Q000494:pharmacology*; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology; D010610:Pharyngeal Neoplasms / Q000473:pathology*; D014176:Protein Biosynthesis; D011691:Puromycin / Q000494:pharmacology; D012313:RNA / Q000096:biosynthesis*
D037102:Lectins; D008937:Mitomycins; D003208:Concanavalin A; D003609:Dactinomycin; D011691:Puromycin; D016685:Mitomycin; D012313:RNA; D004640:Emetine