作者: Roberta Valenti , Veronica Huber , Paola Filipazzi , Manuela Iero , Giorgio Parmiani
DOI: 10.1007/978-0-387-88611-4_8
关键词: Dendritic cell 、 Immune system 、 Biology 、 Cancer cell 、 Dendritic cell differentiation 、 Microvesicles 、 Myeloid 、 Cancer research 、 Antigen 、 Acquired immune system
摘要: Cancer cells constitutively release endosome-derived microvesicles, also called ‘exosomes’, carrying a broad array of molecular determinants involved in the remodeling peritumoral microenvironment. This recently defined alternative mechanism intercellular communication is exploited by tumor to favor their own growth and survival through delivery detrimental signals host’s innate adaptive immune system. Initially described for ability transfer antigens dendritic protected highly immunogenic membrane-embedded form, tumor-derived exosomes have been more hinted exert immunosuppressive effects on development antitumor responses at different levels. In particular, due transport FasL TRAIL pro-apoptotic molecules, derived from histotypes proved induce programmed cell death activated antitumor-specific T cells. On other hand, same microvesicles seem mine immune-mediated recognition elimination cancer since initial stages, regarding antigen uptake presentation As reported herein, patients display several phenotypic functional defects this subset, together with generalized dysfunction myeloid compartment, tumor-driven expansion activation so-called ‘myeloid suppressor cells’. A possible involvement disruption homeostasis antigen-presenting compartment has suggested series experimental evidences, as it will be mainly discussed chapter.