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
Published April 1, 2016
Citation Information: J Clin Invest. 2016;126(4):1173-1180. https://doi.org/10.1172/JCI81131.
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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 3

Modifying EVs for therapeutic applications.

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Modifying EVs for therapeutic applications. APCs can be engineered in cu...
APCs can be engineered in culture to generate immunoregulatory EVs for therapeutic applications. Antigen-specific effects can be achieved by pulsing the APCs with tumor- or pathogen-derived antigens or by transfer of antigen-encoding genes. Similarly, APCs can be modified to express immunosuppressive or immunostimulatory cytokines or ligands, which can render the APC-derived EVs able to suppress or stimulate antigen-specific immune responses. The expression of costimulatory ligands in the APC can result in EVs with increased levels of the ligands, thereby directly affecting the immunoregulatory activity of the EVs. Finally, the EVs themselves can be modified to carry immunomodulatory small RNAs, such as miRNAs or antagomIRs. CTL, cytotoxic T lymphocyte.