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The helminth T2 RNase ω1 promotes metabolic homeostasis in an IL-33– and group 2 innate lymphoid cell–dependent mechanism

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 ω1 (ω1), a potent inducer of type 2 activation, improves metabolic sta...

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Detalles Bibliográficos
Autores principales: Hams, Emily, Bermingham, Rachel, Wurlod, Felicity A., Hogan, Andrew E., O’Shea, Donal, Preston, Roger J., Rodewald, Hans-Reimer, McKenzie, Andrew N. J., Fallon, Padraic G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Federation of American Societies for Experimental Biology 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4973506/
https://www.ncbi.nlm.nih.gov/pubmed/26490658
http://dx.doi.org/10.1096/fj.15-277822
Descripción
Sumario: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 ω1 (ω1), 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 ω1; however, the ability of ω1 to improve metabolic status is reliant upon effective binding of ω1 to CD206. We demonstrate a novel mechanism for RNase-mediated 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 ω1 promotes metabolic homeostasis in an IL-33– and group 2 innate lymphoid cell–dependent mechanism.