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. 2012 Apr 19:3:82.
doi: 10.3389/fimmu.2012.00082. eCollection 2012.

Mast Cells Respond to Cell Injury through the Recognition of IL-33

Carolina Lunderius-Andersson  1 , Mattias Enoksson, Gunnar Nilsson
Affiliations

Mast Cells Respond to Cell Injury through the Recognition of IL-33

Carolina Lunderius-Andersson et al. Front Immunol. .

Abstract

Mast cells have been attributed several functions in both health and disease. Mast cell activation and release of inflammatory mediators are associated with the pathogenesis of several diseases, in particular that of allergic diseases. While the notion of mast cells as important, protective sentinel cells is old, this feature of the cell is not well recognized outside the mast cell field. The mast cell is a unique, multifunctional cell of our defense system, with characteristics such as wide-spread tissue distribution, expression of receptors capable of recognizing both endogenous and exogenous agents, and a capability to rapidly respond to triggering factors by selective mediator release. In this review, we discuss the function of mast cells as sentinel cells in the context of cell injury, where mast cells respond by initiating an inflammatory response. In this setting, IL-33 has turned out to be of particular interest. IL-33 is released by necrotic structural cells and is recognized by mast cells via the IL-33 receptor ST2. IL-33 and mast cells probably constitute one important link between cell injury and an inflammatory response that can lead to restoration of tissue function and homeostasis, but might under other circumstances contribute to a vicious circle driving chronic inflammation.

Keywords: IL-33; IL-6; inflammation; injury; mast cell; migration.

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Figures

Figure 1
Figure 1
IL-33 is a potent regulator of mast cell functions. IL-33 triggers several events in mast cells, including release of cytokines, chemokines, and lipid mediators. In addition, IL-33 has been shown to promote mast cell survival, adhesion, and maturation. While IL-33 does not seem to induce degranulation in naïve mast cells, IL-33 augment IgE-receptor mediated degranulation and cytokine release.
Figure 2
Figure 2
Mast cells respond to IL-33 released during cell injury by initiating a pro-inflammatory response. During cell injury, for instance induced by mechanical trauma, structural cell types such as epithelial cells release IL-33. Mast cells recognize IL-33 through the T1/ST2 receptor, which initiates MyD88-dependent signaling mechanisms eventually resulting in NFkB activation and the subsequent transcription of several pro-inflammatory genes. Release of cytokines, chemokines, and lipid mediators together initiates a inflammatory response, for instance resulting in neutrophil recruitment, activation and migration of dendritic cells, and polarization of T cells.
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References

    1. Abraham S. N., St. John A. L. (2010). Mast cell-orchestrated immunity to pathogens. Nat. Rev. Immunol. 10, 440–45210.1038/nri2782 - DOI - PMC - PubMed
    1. Ali S., Huber M., Kollewe C., Bischoff S. C., Falk W., Martin M. U. (2007). IL-1 receptor accessory protein is essential for IL-33-induced activation of T lymphocytes and mast cells. Proc. Natl. Acad. Sci. U.S.A. 104, 18660–1866510.1073/pnas.0705939104 - DOI - PMC - PubMed
    1. Ali S., Mohs A., Thomas M., Klare J., Ross R., Schmitz M. L., Martin M. U. (2011). The dual function cytokine IL-33 interacts with the transcription factor NF-{kappa}B To dampen NF-{kappa}B-stimulated gene transcription. J Immunol. 187, 1609–161610.4049/jimmunol.1003080 - DOI - PubMed
    1. Ali S., Nguyen D. Q., Falk W., Martin M. U. (2010). Caspase 3 inactivates biologically active full length interleukin-33 as a classical cytokine but does not prohibit nuclear translocation. Biochem. Biophys. Res. Commun. 391, 1512–151610.1016/j.bbrc.2009.12.107 - DOI - PubMed
    1. Allakhverdi Z., Comeau M. R., Jessup H. K., Yoon B. R., Brewer A., Chartier S., Paquette N., Ziegler S. F., Sarfati M., Delespesse G. (2007a). Thymic stromal lymphopoietin is released by human epithelial cells in response to microbes, trauma, or inflammation and potently activates mast cells. J. Exp. Med. 204, 253–25810.1084/jem.20062211 - DOI - PMC - PubMed

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