Il Gruppo di Immunologia  dell'Istituto di Biochimica delle Proteine è lieto di invitarvi all'evento "ImmuNapoli 2016", venerdì 25 novembre p.v. alle 14.30 presso la Sala Conferenze dell'Area della Ricerca CNR Na1 in via Castellino, 111, Napoli. In tale occasione il Prof. Alberto Mantovani, Direttore Scientifico di Humanitas Clinical and Research Center e Professore Ordinario di Patologia presso Humanitas University, Milano, terrà un seminario dal titolo:

"Molecular pathways linking inflammation and cancer: from bench to bedside"

Macrophages are key orchestrators of chronic inflammation. They respond to microenvironmental signals with polarized genetic and functional programmes.   M1 macrophages which are classically activated by microbial products and interferon-γ, are potent effector cells which kill microorganisms and tumours. In contrast, M2 cells tune inflammation and adaptive immunity; promote cell proliferation by producing growth factors and products of the arginase pathway (ornithine and polyamines); scavenge debris by expressing scavenger receptors; promote angiogenesis, tissue remodeling and repair. M1 and M2 cells represent simplified extremes of a continuum of functional states. Available information suggests that some TAM are a prototypic M2 population.  Polarization of phagocytes sets these cells  in a tissue remodeling and repair mode and orchestrate the smouldering and polarized chronic inflammation associated to established neoplasia. Intrinsic metabolic features and orchestration of metabolism are key components of macrophage  polarization and function.  Recent studies have begun to address the central issue of the relationship between genetic events causing cancer and activation of protumour, smouldering, non-resolving tumour-promoting inflammation.  New vistas have emerged on molecules associated with M2 or M2-like polarization and its orchestration in cancer. Recently, proof-of-principle has been obtained that targeting TAM can be beneficial in human cancer. Moreover, complement has emerged as a key component of tumor-promoting inflammation.