The helminth T2 RNase o1 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 o1 (o1) 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 o1; however, the ability of o1 to improve metabolic status is reliant upon effective binding of o1 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 o1 promotes metabolic homeostasis in an IL 33 and group 2 innate lymphoid cell dependent mechanism. FASEB J. 30, 824 835 (2016) www.fasebj.org
FASEB journal official publication of the Federation of American Societies for Experimental Biology