Dissociation between macrophage tumoricidal capacity and suppressive activity: Analysis with macrophage-defective mouse strains

D. Boraschi, E. Pasqualetto, P. Ghezzi, M. Salmona, M. Bartalini, G. Barbarulli, S. Censini, D. Soldateschi, A. Tagliabue

Research output: Contribution to journalArticle

Abstract

Macrophages (Mφ) from three mouse strains with genetically distinct Mφ deficits (C3H/HeJ, A/J, and P/J) were unable to develop high cytolytic and cytotoxic activity against tumor cells in vitro when exposed to agents (MAF and IFN-β) that strongly increased the tumoricidal capacity of Mφ from nondefective C3H/HeN mice. Nevertheless, the tumoricidal deficits of Mφ from the defective strains did not affect their suppressive capacity on Con A-induced lymphoproliferation, nor their ability to react to IFN-β by decreasing suppressive activity. In fact, natural suppressive activity and IFN-β-induced changes in the suppression of Mφ from C3H/HeJ, A/J, and P/J mice were highly comparable to those of C3H/HeN Mφ, thus stressing the dossociation between the mechanisms governing Mφ suppression and M3F tumoricidal activity. Analysis of the modulation by MAF and IFN-β of Mφ ability to release the oxygen metabolites O2 - and H2O2, molecules possibly involved in the effector mechanism of both Mφ cytotoxicity and suppression, revealed a close correlation with the patterns of suppressive activity in both nondefective and defective strains. In contrast, no correlation between the production of oxygen-reactive species and Mφ tumoricidal activity was observed. The ability of MAF- and IFN-β-treated Mφ to produce PGE, a molecule of major importance in Mφ-mediated suppression and possibly involved also in the regulation of Mφ tumoricidal activity, again paralleled Mφ suppressive capacity. Thus, the mechanisms controlling Mφ antitumor activity appeared to be clearly distinct from those involved in Mφ suppression.

Original languageEnglish
Pages (from-to)1707-1713
Number of pages7
JournalJournal of Immunology
Volume131
Issue number4
Publication statusPublished - 1983

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Macrophages
Inbred C3H Mouse
Prostaglandins E
Reactive Oxygen Species
Oxygen
Neoplasms
In Vitro Techniques

ASJC Scopus subject areas

  • Immunology

Cite this

Boraschi, D., Pasqualetto, E., Ghezzi, P., Salmona, M., Bartalini, M., Barbarulli, G., ... Tagliabue, A. (1983). Dissociation between macrophage tumoricidal capacity and suppressive activity: Analysis with macrophage-defective mouse strains. Journal of Immunology, 131(4), 1707-1713.

Dissociation between macrophage tumoricidal capacity and suppressive activity : Analysis with macrophage-defective mouse strains. / Boraschi, D.; Pasqualetto, E.; Ghezzi, P.; Salmona, M.; Bartalini, M.; Barbarulli, G.; Censini, S.; Soldateschi, D.; Tagliabue, A.

In: Journal of Immunology, Vol. 131, No. 4, 1983, p. 1707-1713.

Research output: Contribution to journalArticle

Boraschi, D, Pasqualetto, E, Ghezzi, P, Salmona, M, Bartalini, M, Barbarulli, G, Censini, S, Soldateschi, D & Tagliabue, A 1983, 'Dissociation between macrophage tumoricidal capacity and suppressive activity: Analysis with macrophage-defective mouse strains', Journal of Immunology, vol. 131, no. 4, pp. 1707-1713.
Boraschi, D. ; Pasqualetto, E. ; Ghezzi, P. ; Salmona, M. ; Bartalini, M. ; Barbarulli, G. ; Censini, S. ; Soldateschi, D. ; Tagliabue, A. / Dissociation between macrophage tumoricidal capacity and suppressive activity : Analysis with macrophage-defective mouse strains. In: Journal of Immunology. 1983 ; Vol. 131, No. 4. pp. 1707-1713.
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T2 - Analysis with macrophage-defective mouse strains

AU - Boraschi, D.

AU - Pasqualetto, E.

AU - Ghezzi, P.

AU - Salmona, M.

AU - Bartalini, M.

AU - Barbarulli, G.

AU - Censini, S.

AU - Soldateschi, D.

AU - Tagliabue, A.

PY - 1983

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N2 - Macrophages (Mφ) from three mouse strains with genetically distinct Mφ deficits (C3H/HeJ, A/J, and P/J) were unable to develop high cytolytic and cytotoxic activity against tumor cells in vitro when exposed to agents (MAF and IFN-β) that strongly increased the tumoricidal capacity of Mφ from nondefective C3H/HeN mice. Nevertheless, the tumoricidal deficits of Mφ from the defective strains did not affect their suppressive capacity on Con A-induced lymphoproliferation, nor their ability to react to IFN-β by decreasing suppressive activity. In fact, natural suppressive activity and IFN-β-induced changes in the suppression of Mφ from C3H/HeJ, A/J, and P/J mice were highly comparable to those of C3H/HeN Mφ, thus stressing the dossociation between the mechanisms governing Mφ suppression and M3F tumoricidal activity. Analysis of the modulation by MAF and IFN-β of Mφ ability to release the oxygen metabolites O2 - and H2O2, molecules possibly involved in the effector mechanism of both Mφ cytotoxicity and suppression, revealed a close correlation with the patterns of suppressive activity in both nondefective and defective strains. In contrast, no correlation between the production of oxygen-reactive species and Mφ tumoricidal activity was observed. The ability of MAF- and IFN-β-treated Mφ to produce PGE, a molecule of major importance in Mφ-mediated suppression and possibly involved also in the regulation of Mφ tumoricidal activity, again paralleled Mφ suppressive capacity. Thus, the mechanisms controlling Mφ antitumor activity appeared to be clearly distinct from those involved in Mφ suppression.

AB - Macrophages (Mφ) from three mouse strains with genetically distinct Mφ deficits (C3H/HeJ, A/J, and P/J) were unable to develop high cytolytic and cytotoxic activity against tumor cells in vitro when exposed to agents (MAF and IFN-β) that strongly increased the tumoricidal capacity of Mφ from nondefective C3H/HeN mice. Nevertheless, the tumoricidal deficits of Mφ from the defective strains did not affect their suppressive capacity on Con A-induced lymphoproliferation, nor their ability to react to IFN-β by decreasing suppressive activity. In fact, natural suppressive activity and IFN-β-induced changes in the suppression of Mφ from C3H/HeJ, A/J, and P/J mice were highly comparable to those of C3H/HeN Mφ, thus stressing the dossociation between the mechanisms governing Mφ suppression and M3F tumoricidal activity. Analysis of the modulation by MAF and IFN-β of Mφ ability to release the oxygen metabolites O2 - and H2O2, molecules possibly involved in the effector mechanism of both Mφ cytotoxicity and suppression, revealed a close correlation with the patterns of suppressive activity in both nondefective and defective strains. In contrast, no correlation between the production of oxygen-reactive species and Mφ tumoricidal activity was observed. The ability of MAF- and IFN-β-treated Mφ to produce PGE, a molecule of major importance in Mφ-mediated suppression and possibly involved also in the regulation of Mφ tumoricidal activity, again paralleled Mφ suppressive capacity. Thus, the mechanisms controlling Mφ antitumor activity appeared to be clearly distinct from those involved in Mφ suppression.

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