Deciphering the role of interleukin-22 in metabolic alterations
© Sabat and Wolk. 2015
Received: 25 November 2015
Accepted: 4 December 2015
Published: 15 December 2015
Inflammatory processes and metabolic alterations are supposed to substantially interact. Recently, cumulating reports describe a profound role of interleukin(IL)-22 in this relationship. IL-22 is a particular kind of immune mediator that is produced by certain lymphocyte populations and regulates the function of several tissue cells but not immune cells. So far, IL-22 was known to plays a fundamental role in the elimination of bacterial infections at border surfaces of the body and to protect tissues from damage. This research highlight article arranges the facts regarding the effects of IL-22 in the context of adiposity and metabolic alterations and postulates a new function of the immune system.
KeywordsObesity Metabolic alterations Immunity Th1-cells Th17-cells Th22-cells ILC3 Diabetes mellitus Arteriosclerosis IL-17 TNF-α
The IL-22/IL-22R1 system
Role of endogenous IL-22 in the development of adiposity and metabolic alterations
IL-22 as therapeutic agent for adiposity and metabolic alterations
group 3 innate lymphoid cell
high fat diet
type 2 diabetes mellitus
Both authors designed and wrote the manuscript. Both authors read and approved the final manuscript.
RS is supported among others by Deutsche Forschungsgemeinschaft (German Research Foundation) (SA 1868/2–1).
The authors declare that they have no competing interests.
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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