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mTORC2 signalling regulates M2 macrophage differentiation in response to helminth infection and adaptive thermogenesis

Hallowell, R. W., Collins, S. L., Craig, J. M., Zhang, Y., Oh, M., Illei, P. B., Chan-Li, Y., Vigeland, C. L., Mitzner, W., Scott, A. L., Powell, J. D., Horton, M. R.·2017·Nature Communications
DOI 10.1038/ncomms14208PMC PMC5290163
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Abstract

Alternatively activated macrophages (M2) have an important function in innate immune responses to parasitic helminths, and emerging evidence also indicates these cells are regulators of systemic metabolism. Here we show a critical role for mTORC2 signalling in the generation of M2 macrophages. Abrogation of mTORC2 signalling in macrophages by selective conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 macrophages while leaving the generation of classically activated macrophages (M1) intact. Selective deletion of Rictor in macrophages prevents M2 differentiation and clearance of a parasitic helminth infection in mice, and also abrogates the ability of mice to regulate brown fat and maintain core body temperature. Our findings define a role for mTORC2 in macrophages in integrating signals from the immune microenvironment to promote innate type 2 immunity, and also to integrate systemic metabolic and thermogenic responses.

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Metadata

Authors
Hallowell, R. W., Collins, S. L., Craig, J. M., Zhang, Y., Oh, M., Illei, P. B., Chan-Li, Y., Vigeland, C. L., Mitzner, W., Scott, A. L., Powell, J. D., & Horton, M. R.
Venue
Nature Communications
Publisher
Springer Science and Business Media LLC
Published
2017-01-27
Volume
8
Issue
1
ISSN
2041-1723
DOI
10.1038/ncomms14208
PMC
PMC5290163
Cited by
129
References
6
Language
en
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