Regulation of chronic inflammatory and immune processes by extracellular vesicles
Paul D. Robbins, Akaitz Dorronsoro, Cori N. Booker
Paul D. Robbins, Akaitz Dorronsoro, Cori N. Booker
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Review Series

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Abstract

Almost all cell types release extracellular vesicles (EVs), which are derived either from multivesicular bodies or from the plasma membrane. EVs contain a subset of proteins, lipids, and nucleic acids from the cell from which they are derived. EV factors, particularly small RNAs such as miRNAs, likely play important roles in cell-to-cell communication both locally and systemically. Most of the functions associated with EVs are in the regulation of immune responses to pathogens and cancer, as well as in regulating autoimmunity. This Review will focus on the different modes of immune regulation, both direct and indirect, by EVs. The therapeutic utility of EVs for the regulation of immune responses will also be discussed.

Authors

Paul D. Robbins, Akaitz Dorronsoro, Cori N. Booker

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Figure 2

Role of endogenous EVs in regulating immune responses.

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Role of endogenous EVs in regulating immune responses. (A) Resident APCs...
(A) Resident APCs, such as macrophages in the tumor environment, can acquire tumor antigens either by uptake of tumor EVs or by phagocytosis of necrotic tumor cells. APCs then release MHC class II+ EVs into the circulation that are able to interact with immune cells at distant sites to suppress tumor antigen-specific immune responses; these are termed tolerogenic EVs. (B) Infection with a pathogen or immunization to an antigen results in acquisition of antigen by local APCs, followed by release of APC-derived EVs into the circulation. APC-derived EVs can carry the antigen and/or present antigen-derived epitopes in MHC class I and MHC class II complexes. Circulating EVs are taken up by APCs in the spleen or lymph nodes where they can modulate immune response to the antigen. It is hypothesized that these vesicles act to suppress the systemic immune response to the antigen or infection to limit the extent of inflammation or autoimmunity.