Wounds that heal and wounds that don't - The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

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Wounds that heal and wounds that don't - The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

Millar, Neal L.; O'Donnell, Charlotte; McInnes, Iain B.; Brint, Elizabeth K.
Date: 2016-08
Copyright: © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
Copyright information: http://creativecommons.org/licenses/by-nc-nd/4.0/
Related: http://www.sciencedirect.com/science/article/pii/S1084952116302452
Full text restriction information: Access to this article is restricted until 12 months after publication by the request of the publisher.
Restriction lift date: 2017-08-10
Citation: Millar, N. L., O’Donnell, C., McInnes, I. B. and Brint, E. (2017) ‘Wounds that heal and wounds that don’t − The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis’, Seminars in Cell and Developmental Biology, 61, pp. 41-50. doi: 10.1016/j.semcdb.2016.08.007
Published Version: 10.1016/j.semcdb.2016.08.007

Abstract:

IL-33 is a member of the IL-1 family of cytokines. IL-33 is predominantly located within the nucleus of cells where it plays a role in gene regulation. Given the right combination of signals and cellular damage, stored IL-33 is released from the cell where it can interact with its receptor ST2, triggering danger-associated responses and act as a cellular "alarmin". Whilst IL-33/ST2 signalling has been shown to induce potent pro-inflammatory responses that can be detrimental in certain disease states, a dichotomous, protective role of IL-33 in promoting wound healing has also emerged in multiple tissues types. This review will explore the current literature concerning this homeostatic role of IL-33/ST2 in tissue repair and also review its role in uncontrolled wound responses as seen in both fibrosis and tumorigenesis.

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© 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license Except where otherwise noted, this item's license is described as © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
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