TY - JOUR T1 - Involvement of Pattern Recognition Receptors in the Induction of Cytokines and Reactive Oxygen Intermediates Production by Human Monocytes/Macrophages Stimulated with Tumour Cells JF - Anticancer Research JO - Anticancer Res SP - 2287 LP - 2294 VL - 24 IS - 4 AU - BOZENNA MYTAR AU - MARIA WOLOSZYN AU - ANNA MACURA-BIEGUN AU - BARBARA HAJTO AU - IRENA RUGGIERO AU - BARBARA PIEKARSKA AU - MAREK ZEMBALA Y1 - 2004/07/01 UR - http://ar.iiarjournals.org/content/24/4/2287.abstract N2 - Background: Some ligands of pattern recognition receptors (PRR) are present on tumour cells. The role of PRR in signalling for cytokine and reactive oxygen intermediates (ROI) production by monocytes and monocyte-derived macrophages (MDM) stimulated with tumour cells was studied. Materials and Methods: Monocytes/MDM were pretreated with PRR ligands or anti-PRR monoclonal antibodies (mAbs) and stimulated with tumour cells. Cytokine secretion was measured by enzyme-linked immunoassay (ELISA) and ROI production by luminol-dependent chemiluminescence (CL). Results: The ligands of scavenger receptor A (SR-A): (fucoidan, polyguanylic acid (polyG) and modified low density lipoproteins (LDL)) and B (SR-B) (native and modified LDL, phosphatidylserine (PdS)) and of mannose receptor (MR) (mannan), induced tumour necrosis factor alpha (TNF) and ROI (except LDL) release by monocytes. Production of TNF and interleukin-10 (IL-10) by MDM was stimulated by SR-A ligands and mannan. Tumour cell-induced TNF and IL-10 production by monocytes, but not MDM, was diminished by fucoidan and polyG, while ROI release was reduced by MR and SR-A ligands. Supplementation of tumour cells with modified LDL and PdS enhanced their stimulatory capacity. TNF and ROI release by tumour cells-stimulated monocytes was inhibited by anti-CD36 and anti-MR (clone PAM-1) mAbs. Conclusion: SR and MR may be involved to different extents in the induction of cytokines and ROI production by monocytes, but not MDM, stimulated with tumour cells. Copyright© 2004 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved ER -