Hams, Emily and Bermingham, Rachel and Wurlod, Felicity A. and Hogan, Andrew E. and O'Shea, Donal and Preston, Roger J. and Rodewald, Hans-Reimer and McKenzie, Andrew N.J. and Fallon, Padraic G.
(2016)
The helminth T2 RNase v1 promotes metabolic
homeostasis in an IL-33– and group 2 innate lymphoid
cell–dependent mechanism.
The FASEB Journal, 30.
pp. 824-835.
ISSN 0892-6638
Abstract
Induction of a type 2 cellular response in
the white adipose tissue leads to weight loss and improves
glucose homeostasis in obese animals. Injection of obese
mice with recombinant helminth-derived Schistosoma mansoni
egg-derived v1 (v1), a potent inducer of type 2 activation, improves metabolic status involving a mechanism
reliant upon release of the type 2 initiator cytokine IL-33.
IL-33 initiates the accumulation of group 2 innate lymphoid cells (ILC2s), eosinophils, and alternatively activated macrophages in the adipose tissue. IL-33 release
from cells in the adipose tissue is mediated by the RNase
activity of v1; however, the ability of v1 to improve metabolic status is reliant upon effective binding of v1 to
CD206. We demonstrate a novel mechanism for RNasemediated release of IL-33 inducing ILC2-dependent improvements in the metabolic status of obese animals.—
Hams, E., Bermingham, R., Wurlod, F. A., Hogan, A. E.,
O’Shea, D., Preston, R. J., Rodewald, H.-R., McKenzie,
A. N. J., Fallon, P. G. The helminth T2 RNase v1 promotes metabolic homeostasis in an IL-33– and group 2
innate lymphoid cell–dependent mechanism.
Item Type: |
Article
|
Keywords: |
obesity; adipocytes; inflammation; |
Academic Unit: |
Faculty of Science and Engineering > Biology |
Item ID: |
12402 |
Identification Number: |
https://doi.org/10.1096/fj.15-277822 |
Depositing User: |
Andrew Hogan
|
Date Deposited: |
10 Feb 2020 17:44 |
Journal or Publication Title: |
The FASEB Journal |
Publisher: |
Federation of American Society of Experimental Biology |
Refereed: |
Yes |
URI: |
|
Use Licence: |
This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available
here |
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