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 language | English |
|---|---|
| Pages (from-to) | 1707-1713 |
| Number of pages | 7 |
| Journal | Journal of Immunology |
| Volume | 131 |
| Issue number | 4 |
| Publication status | Published - 1983 |
Fingerprint
ASJC Scopus subject areas
- Immunology
Cite this
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 journal › Article
}
TY - JOUR
T1 - Dissociation between macrophage tumoricidal capacity and suppressive activity
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
Y1 - 1983
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.
UR - http://www.scopus.com/inward/record.url?scp=0020555992&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0020555992&partnerID=8YFLogxK
M3 - Article
C2 - 6311895
AN - SCOPUS:0020555992
VL - 131
SP - 1707
EP - 1713
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 4
ER -