Abstract
In addition to being major effector cells in the elicitation of allergic responses, mast cells have been found to play a significant role in the establishment of innate and adaptive immune responses. This occurs, in part, by regulating the phenotype and function of immune cells such as T cells, B cells and dendritic cells, and by acting as antigen presenting cells. Indeed, mast cells have been found to be activated in various T cell-mediated inflammatory processes and to reside in close physical proximity to T cells. Such observations have led investigators to propose a functional relationship between these two cell populations. Mast cells can interact with other cells including T cells in several ways such as cell-cell interaction via membrane associated receptors, release of cytokines and chemokines or by heterotypic adhesion to activated T cells. In this review, we focus on a novel communication pathway between mast cells and other inflammatory cells that occurs by the release of or response to membrane vesicles. Membrane vesicles are circular fragments, released from the endosomal compartment as exosomes or shed from the cell plasma membrane as microparticles. Because their membrane orientation is the same as that of the donor cell, they can be considered to be miniature versions of a cell. Growing evidence indicates that microparticles play a pivotal role in cell to cell communication. The functional consequences of such membrane transfers include the induction, amplification and/or modulation of immune responses, as well as the acquisition of new functional properties by recipient cells.
Keywords: Exosomes, cell membrane/ultrastructure, cell membrane/physiology, microparticles, microvesicles, T cells, inflammation, membrane vesicles, immunosuppression, cytokines
Current Pharmaceutical Design
Title: Mast Cells as Sources and Targets of Membrane Vesicles
Volume: 17 Issue: 34
Author(s): Irit Shefler, Pazit Salamon, Alon Y. Hershko and Yoseph A. Mekori
Affiliation:
Keywords: Exosomes, cell membrane/ultrastructure, cell membrane/physiology, microparticles, microvesicles, T cells, inflammation, membrane vesicles, immunosuppression, cytokines
Abstract: In addition to being major effector cells in the elicitation of allergic responses, mast cells have been found to play a significant role in the establishment of innate and adaptive immune responses. This occurs, in part, by regulating the phenotype and function of immune cells such as T cells, B cells and dendritic cells, and by acting as antigen presenting cells. Indeed, mast cells have been found to be activated in various T cell-mediated inflammatory processes and to reside in close physical proximity to T cells. Such observations have led investigators to propose a functional relationship between these two cell populations. Mast cells can interact with other cells including T cells in several ways such as cell-cell interaction via membrane associated receptors, release of cytokines and chemokines or by heterotypic adhesion to activated T cells. In this review, we focus on a novel communication pathway between mast cells and other inflammatory cells that occurs by the release of or response to membrane vesicles. Membrane vesicles are circular fragments, released from the endosomal compartment as exosomes or shed from the cell plasma membrane as microparticles. Because their membrane orientation is the same as that of the donor cell, they can be considered to be miniature versions of a cell. Growing evidence indicates that microparticles play a pivotal role in cell to cell communication. The functional consequences of such membrane transfers include the induction, amplification and/or modulation of immune responses, as well as the acquisition of new functional properties by recipient cells.
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Cite this article as:
Shefler Irit, Salamon Pazit, Y. Hershko Alon and A. Mekori Yoseph, Mast Cells as Sources and Targets of Membrane Vesicles, Current Pharmaceutical Design 2011; 17 (34) . https://dx.doi.org/10.2174/138161211798357836
DOI https://dx.doi.org/10.2174/138161211798357836 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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