Abstract
Extracellular vesicles (EVs) are increasingly understood to participate directly in many essential aspects of host antitumor immune response. Tumor- and immune-cell-derived EVs function in local and systemic contexts with roles in immune processes including cancer antigen conveyance, immune cell priming and activation, as well as immune escape. Current practice of cancer immunotherapy has de facto focused on eliciting T-cell-mediated cytotoxic responses. Humoral immunity is also known to exert antitumor effects, and B cells have been demonstrated to have functions that extend beyond antibody production to include antigen presentation and activation and modulation of T cells and innate immune effectors. Evidence of B cell response against tumor-associated antigens (TAAs) is observed in early stages of tumorigenesis and in most solid tumor types. It is known that EVs convey diverse TAAs, express antigenic-peptide-loaded MHCs, and complex with circulating plasma antitumoral autoantibodies. In this review, we will consider the relationships between EVs, B cells, and other antigen-presenting cells, especially in relation to TAAs. Understanding the intersection of EVs and the cancer immunome will enable opportunities for developing tumor antigen targets, antitumor vaccines and harnessing the full potential of multiple immune system components for next-generation cancer immunotherapies.
Highlights
Converging lines of evidence reveal extracellular vesicles (EVs) as important mediators of tumor-immune interchange [1,2,3,4,5]
The findings suggest EVs as a compelling target for antitumor intervention, both as a means to guide existing modes of immunotherapy through interrogation of tumor surface antigens or status of immune infiltrate, or as a novel target for interception and reversal of cancer cell signaling in relation to immune tolerance
A few factors regulate the potency of MHC cross-dressing of antigen-presenting cells (APCs) via EVs, and acceptor APCs behave as platforms that intensify the capacity of the EVs generated to express peptide-MHCs straight to T cells
Summary
Converging lines of evidence reveal extracellular vesicles (EVs) as important mediators of tumor-immune interchange [1,2,3,4,5]. Profiling tumor-derived EVs (TDEs) reveals a diverse repertoire of tumor-associated antigens (TAAs) and functional effectors of humoral and cellular immunity [6]. A few factors regulate the potency of MHC cross-dressing of APCs via EVs, and acceptor APCs behave as platforms that intensify the capacity of the EVs generated to express peptide-MHCs straight to T cells This EV-mediated move as well as membrane microdomains, such as sphingolipid-enriched lipid rafts and caveolae, and diverse molecular cargoes including nucleic acids, metabolites, and proteins [18]. In another study progression of castration-resistant prostate cancer was associated with B cell infiltration and activation of IKKα, which stimulates metastasis by an NF-κB-independent mechanism [29] These data suggest spatiotemporal and context-dependent aspects of tumor and B cell interactions have yet to be fully understood
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