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

Overview

Journal Front Immunol

Specialty Allergy & Immunology

Date 2012 May 9

PMID 22566963

Citations 48

Authors

Carolina Lunderius-Andersson

Mattias Enoksson

Gunnar Nilsson

Affiliations

Soon will be listed here.

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.

Citing Articles

IL-33 signaling is dispensable for the IL-10-induced enhancement of mast cell responses during food allergy.

Krajewski D, Ranjitkar S, Jordan N, Schneider S, Mathias C Front Immunol. 2025; 16:1526498.

PMID: 39935481 PMC: 11810977. DOI: 10.3389/fimmu.2025.1526498.

IL-33-primed human mast cells drive IL-9 production by CD4 effector T cells in an OX40L-dependent manner.

Battut L, Leveque E, Valitutti S, Cenac N, Dietrich G, Espinosa E Front Immunol. 2024; 15:1470546.

PMID: 39416773 PMC: 11479898. DOI: 10.3389/fimmu.2024.1470546.

Associations of gene variants, IL-33, and sST2 with the risk of Henoch-Schönlein purpura in children.

Ruan Y, Xie L Heliyon. 2024; 10(8):e29469.

PMID: 38655333 PMC: 11036003. DOI: 10.1016/j.heliyon.2024.e29469.

Longitudinal cytokine and multi-modal health data of an extremely severe ME/CFS patient with HSD reveals insights into immunopathology, and disease severity.

Jahanbani F, Sing J, Maynard R, Jahanbani S, Dafoe J, Dafoe W Front Immunol. 2024; 15:1369295.

PMID: 38650940 PMC: 11033372. DOI: 10.3389/fimmu.2024.1369295.

IL-10 Differentially Promotes Mast Cell Responsiveness to IL-33, Resulting in Enhancement of Type 2 Inflammation and Suppression of Neutrophilia.

Ranjitkar S, Krajewski D, Garcia C, Tedeschi C, Polukort S, Rovatti J J Immunol. 2024; 212(9):1407-1419.

PMID: 38497670 PMC: 11018500. DOI: 10.4049/jimmunol.2300884.

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