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Semin Immunol. 2015 May;27(3):161-8. doi: 10.1016/j.smim.2015.05.003. Epub 2015 May 30.

New insights into the resolution of inflammation.

Author information

1
Centre for Clinical Pharmacology and Therapeutics, Division of Medicine, 5 University Street, University College London, London WC1E 6JJ, United Kingdom. Electronic address: d.gilroy@ucl.ac.uk.
2
Centre for Clinical Pharmacology and Therapeutics, Division of Medicine, 5 University Street, University College London, London WC1E 6JJ, United Kingdom.

Abstract

The goal of treating chronic inflammatory diseases must be to inhibit persistent inflammation and restore tissue function. To achieve this we need to improve our understanding of the pathways that drive inflammation as well as those that bring about its resolution. In particular, resolution of inflammation is driven by a complex set of mediators that regulate cellular events required to clear inflammatory cells from sites of injury or infection and restore homeostasis. Indeed, it may be argued that dysfunctional resolution may underpin the aetiology of some chronic inflammatory disease and that a novel goal in treating such diseases is to develop drugs based on the mode of endogenous pro-resolution factors in order to drive on-going inflammation down a pro-resolution pathway. And while we are improving our understanding of the resolution of acute and chronic inflammation, much remains to be discovered. Here we will discuss the key endogenous checkpoints necessary for mounting an effective yet limited inflammatory response and the crucial biochemical pathways necessary to prevent its persistence and trigger its resolution. In doing so, we will provide an update on what is known about resolution of acute inflammation, in particular its link with adaptive immunity.

KEYWORDS:

Adaptive immunity; Chronic inflammation; Eicosanoids; Macrophages

PMID:
26037968
DOI:
10.1016/j.smim.2015.05.003
[Indexed for MEDLINE]

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