Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10941045 | Immunobiology | 2012 | 8 Pages |
Abstract
Extensive research in the last two decades implemented that the inflammatory cell infiltrate, especially in solid tumors, is a major determinant for patient prognosis. Mononuclear phagocytes, i.e. monocytes/macrophages, dendritic cells and myeloid-derived suppressor cells, constitute the majority of tumor-associated immune cells. Instead of inducing anti-tumor immunity, mononuclear phagocytes are functionally subverted by tumor microenvironmental factors to support each stage of oncogenesis. Although mechanisms how tumors program their inflammatory infiltrate to support tumor development are ill-defined, few master regulators are beginning to emerge. One of them is the inflammatory eicosanoid prostaglandin E2 (PGE2), produced by tumor cells or the infiltrating immune cells. In this review we summarize the impact of PGE2 on mononuclear phagocytes in inflammation and cancer and discuss potential implications for cancer therapy.
Keywords
PGESPGE2APCGPCRNSAIDPDCCDCIDO15-PGDHPLA2CTLMDSCPlasmacytoid DCPGE2 receptorCOXLPSFLT3-LTGF-βnuclear factor ‘kappa-light-chain-enhancer’ of activated B-cellsNF-κBconventional DCcAMPROSCyclic adenosine monophosphateadenomatous polyposis colicyclooxygenasephospholipase A2inflammationinterferonIFNinterleukinindoleamine 2,3-dioxygenaseTAMtransforming growth factor-βtumor necrosis factor-αCancerTh cellDendritic cellmyeloid-derived suppressor cellNon-steroidal anti-inflammatory drugTNF-αcytotoxic lymphocytelipopolysaccharideMacrophageTumor-associated macrophagebone marrowNitric oxideProstaglandin E2LipidsReactive oxygen speciesG protein-coupled receptor
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Authors
Weixiao Sha, Bernhard Brüne, Andreas Weigert,