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• W1994675282 abstract "Tumor growth enhances macrophage (Mφ) suppressor activity by causing Mφ to increase synthesis of inhibitory molecules such as prostaglandin E2 (PGE2) or decreasing their expression of up-regulatory molecules such as the class II MHC protein Ia. Although these tumor-induced changes are correlated, it is unknownwhether tumor-bearing host (TBH) Ia− Mφ become more suppressive by increasing their PGE2 synthesis. To assess the role of PGE2 in tumor-induced Ia− Mφ-mediated suppression of CD4+ T-cell alloreactivity, unseparated (Ia+ -enriched) or Ia+ -depleted (Ia−) populations of murine normal host (NH) or TBH splenic Mφ were added to mixed lymphocyte reaction (MLR) cultures. NH or TBH Ia− Mφ were significantly more suppressive than their respective unseparated populations, and TBH Ia− Mφ were more suppressive than their NH counterparts. When PGE2 production was blocked with indomethacin, TBH Ia− Mφ-mediated suppression was reduced more than suppression mediated by all other Mφ populations. A PGE2-specific ELISA showed more PGE2 in Ia− Mφ-containing cultures than in those with whole Mφ and more cultures containing TBH Ia− Mφ than in their NH counterparts. Because interferon-γ (IFN-γ) is a potent Mφ activation molecule that regulates both Ia expression and PGE2 production, the effects of IFN-γ on tumor-induced Ia− Mφ-mediated suppression were investigated. Exogenous IFN-γ reduced suppression mediated by all Mφ populations except NH unseparated Mφ. IFN-γ suppressed alloreactivity without Mφ or with NH unseparated Mφ. Suppression mediated by NH or TBH Ia−, and TBH unseparated Mφ was also reduced when Mφ were pre-incubated with IFN-γ before their addition to MLR cultures. IFN-γ addition did not block Ia− Mφ-mediated suppression by decreasing Mφ PGE2 production. In fact, IFN-γ addition increased PGE2 production two-fold in MLR cultures. However, IFN-γ partly reduced suppression mediated by exogenous PGE2 added to Mφ-depleted cultures. Cytofluorometric analysis showed that IFN-γ increased the percentage of Ia+ Mφ in NH and TBH Ia− Mφ populations. Blocking TNF-α activity with anti-TNF-α antibodies caused IFN-γ to suppress alloreactivity in all Mφ-added cultures. Collectively, these data show that tumor-induced suppression mediated by Ia− Mφ is caused by increased PGE2 synthesis. IFN-γ strongly reduces Ia− Mφ-mediated suppression by blocking PGE2-mediated suppression, enhancing Ia− Mφ production of the up-regulatory molecule TNF-α, and possibly by increasing the number of Ia+ Mφ. These effects of IFN-γ on Ia− Mφ suggest that this cytokine increases immunity and Mφ-mediated cytotoxicity during cancer." @default.
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• W1994675282 date "1993-05-01" @default.
• W1994675282 modified "2023-09-23" @default.
• W1994675282 title "Interferon-γ reduces tumor-induced Ia− macrophage-mediated suppression: role of prostaglandin E2, Ia, and tumor necrosis factor-α" @default.
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• W1994675282 doi "https://doi.org/10.1016/0162-3109(93)90050-z" @default.
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