Rapid killing of actinomycin D-treated tumour cells by mononuclear phagocytes: Reactivity in mouse strains with defective classical tumour cytotoxicity

F. Collota, L. Bersani, N. Polentarutti, A. Mantovani

Research output: Contribution to journalArticlepeer-review

Abstract

In conformation of previous data, macrophages from C3H/HeJ, C57BL/10ScCR and A/J mice, exposed in vivo to BCG or in vitro to lymphokines, had little tumoricidal activity, as assessed in a 48-hr [3H]thymidine release assay against TU5 tumour cells, compared to macrophages from C3H/HeN, C57BL/6 and BALB/c x DBA/2)F1 mice. Macrophages from these mouse strains were examined for their capacity to kill actinomycin D-pretreated WEHI 164 sarcoma cells in a 6-hr 51chromium release assay (drug-dependent cellular cytotoxicity, DDCC). Peptone-elicited macrophages from C3H/HeN, C57BL/6, (BALB/c x DBA/2(F1, C57BL/10ScCR and A/J mice had high DDCC activity, whereas C3H/HeJ macrophages expressed little cytotoxicity against actinomycin D-pretreated WEHI 164 cells. In vivo exposure to BCG or inactivated streptococci caused a modest augmentation of the DDCC effector function of C3H/HeJ macrophages, but levels of reactivity remained 20-fold less than those of similarly treated normal mice. Thus, C57BL/10ScCR and A/J macrophages have defective classical direct cytotoxicity but mediate DDCC efficiently, whereas C3H/HeJ macrophages are defective in both effector functions.

Original languageEnglish
Pages (from-to)249-253
Number of pages5
JournalImmunology
Volume57
Issue number2
Publication statusPublished - 1986

ASJC Scopus subject areas

  • Immunology

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