PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR γ (PPARγ) LIGANDS REVERSE CTL SUPPRESSION BY ALTERNATIVELY ACTIVATED (M2) MACROPHAGES IN CANCER Running title: Modulating M2-mediated suppression in cancer

作者： Kurt De Groeve , Sofie Meerschaut , Geert Raes , Yuanqing Liu , Jo A Van Ginderachter

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摘要: ABSTRACT Tumors may escape from immune control by the induction of CD11b + Gr-1 myeloid suppressor cells in spleen. In this study, we demonstrate that cell population can be subdivided a hi int SSC lo Ly6G neg M-CSFR immature monocytic fraction and hi+ granulocytic fraction. Upon culture, vitro is sufficient for CTL suppression, linked to their gradual differentiation into mature F4/80 CD68 macrophages. These CTL-suppressive macrophages are alternatively activated (M2), as demonstrated expression known novel M2 signature genes. search M2-associated genes involved suppressive activity, it shown stimulation peroxisome proliferator-activated receptor γ (PPARγ) inhibition phospholipase A 2 (PLA ) activity co-operate alleviate suppression. Importantly, purified tumor-associated display similar phenotype anti-tumor CTLs, via mechanism which almost completely reversed PPARγ ligands. Overall, our data identify PLA

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PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR γ (PPARγ) LIGANDS REVERSE CTL SUPPRESSION BY ALTERNATIVELY ACTIVATED (M2) MACROPHAGES IN CANCER Running title: Modulating M2-mediated suppression in cancer

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PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR γ (PPARγ) LIGANDS REVERSE CTL SUPPRESSION BY ALTERNATIVELY ACTIVATED (M2) MACROPHAGES IN CANCER Running title: Modulating M2-mediated suppression in cancer

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