Abstract
Innate immune cells are recognized for their rapid and critical contribution to the body’s first line of defense against invading pathogens and harmful agents. These actions can be further amplified by specific adaptive immune responses adapted to the activating stimulus. Recently, the awareness has grown that virtually all innate immune cells, i.e., mast cells, neutrophils, macrophages, eosinophils, basophils, and NK cells, are able to communicate with dendritic cells (DCs) and/or T and B cells, and thereby significantly contribute to the orchestration of adaptive immune responses. The means of communication that are thus far primarily associated with this function are cell-cell contacts and the release of a broad range of soluble mediators. Moreover, the possible contribution of innate immune cell-derived extracellular vesicles (EVs) to the modulation of adaptive immunity will be outlined in this review. EVs are submicron particles composed of a lipid bilayer, proteins, and nucleic acids released by cells in a regulated fashion. EVs are involved in intercellular communication between multiple cell types, including those of the immune system. A good understanding of the mechanisms by which innate immune cell-derived EVs influence adaptive immune responses, or vice versa, may reveal novel insights in the regulation of the immune system and can open up new possibilities for EVs (or their components) in controlling immune responses, either as a therapy, target, or as an adjuvant in future immune modulating treatments.
Highlights
For a long time, it has been a general principle in immunology that the development of effector T cells (Th1, Th2, Th17, or regulatory T cells) is directly driven by antigen-primed dendritic cells (DCs) [1]
Based on the summarized literature in this review, it is becoming clear that the extracellular vesicles (EVs) released by different innate immune cells can significantly influence the course of adaptive immune responses or may at least have the capacity to do so based on their cargo
Since the nature of the activating stimulus can significantly affect the content and biological functions of released EVs, their capacity to either enhance or inhibit adaptive immunity may significantly alter when isolated after culturing innate immune cells under suppressive or inflammatory conditions that are far unexplored
Summary
It has been a general principle in immunology that the development of effector T cells (Th1, Th2, Th17, or regulatory T cells) is directly driven by antigen-primed dendritic cells (DCs) [1] It is more and more recognized that both at inflammatory sites and in secondary lymphoid structures, DCs can interact with innate immune cells Mechanisms that are involved in the cross-talk between innate and adaptive immunity obviously include cell-cell contacts and the release of a diverse array of soluble factors, including cytokines and chemokines. Another increasingly investigated and appreciated mechanism via which cells may exert their modulatory effect is through the release of extracellular vesicles (EVs). Efforts have been made to standardize EVrelated experimental methods and documentation [31, 32], and to improve the interpretation of the reviewed data, we concisely indicated the EV isolation methods (i.e., pelleting speed, possibly followed by density gradient ultracentrifugation (DGC)) that were used to obtain the described EV content or their immune modulatory effects
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