title: Immunology in the clinic review series; focus on cancer: tumour-associated macrophages: undisputed stars of the inflammatory tumour microenvironment.
abstract: Mononuclear phagocytes are cells of the innate immunity that defend the host against harmful pathogens and heal tissues after injury. Contrary to expectations, in malignancies, tumour-associated macrophages (TAM) promote disease progression by supporting cancer cell survival, proliferation and invasion. TAM and related myeloid cells [Tie2(+) monocytes and myeloid-derived suppressor cells (MDSC)] also promote tumour angiogenesis and suppress adaptive immune responses. These divergent biological activities are mediated by macrophages/myeloid cells with distinct functional polarization, which are ultimately dictated by microenvironmental cues. Clinical and experimental evidence has shown that cancer tissues with high infiltration of TAM are associated with poor patient prognosis and resistance to therapies. Targeting of macrophages in tumours is considered a promising therapeutic strategy: depletion of TAM or their 're-education' as anti-tumour effectors is under clinical investigation and will hopefully contribute to the success of conventional anti-cancer treatments.
authors.affiliation: Department of Immunology and Inflammation, IRCCS Humanitas Clinical Institute Department of Translational Medicine, University of Milan, Milan, Rozzano, Italy. paola.allavena@humanitasresearch.it
authors.forename: P
authors.initials: P
authors.lastname: Allavena
authors.forename: A
authors.initials: A
authors.lastname: Mantovani
mesh_terms: D000818:Animals; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D017209:Apoptosis / Q000276:immunology; D001557:Benzenesulfonates / Q000008:administration & dosage; D002633:Chemotaxis; D004002:Clodronic Acid / Q000008:administration & dosage / Q000627:therapeutic use; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000502:physiology / Q000627:therapeutic use; D004149:Dioxoles / Q000627:therapeutic use; D018450:Disease Progression; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation; D008081:Liposomes; D008264:Macrophages / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D058990:Molecular Targeted Therapy; D009361:Neoplasm Invasiveness / Q000276:immunology / Q000473:pathology; D009363:Neoplasm Proteins / Q000502:physiology; D009369:Neoplasms / Q000188:drug therapy / Q000276:immunology / Q000473:pathology*; D009389:Neovascularization, Pathologic / Q000276:immunology / Q000473:pathology; D009536:Niacinamide / Q000031:analogs & derivatives; D010671:Phenylurea Compounds; D011379:Prognosis; D011725:Pyridines / Q000008:administration & dosage; D000077157:Sorafenib; D044005:Tetrahydroisoquinolines / Q000627:therapeutic use; D000077606:Trabectedin; D019139:Tumor Escape / Q000187:drug effects / Q000276:immunology; D059016:Tumor Microenvironment / Q000276:immunology*
chemical_list: D001557:Benzenesulfonates; D016207:Cytokines; D004149:Dioxoles; D008081:Liposomes; D009363:Neoplasm Proteins; D010671:Phenylurea Compounds; D011725:Pyridines; D044005:Tetrahydroisoquinolines; D004002:Clodronic Acid; D009536:Niacinamide; D000077157:Sorafenib; D000077606:Trabectedin