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

R. W. Hallowell, S. L. Collins, J. M. Craig, Y. Zhang, M. Oh, P. B. Illei, Y. Chan-Li, C. L. Vigeland, W. Mitzner, A. L. Scott, J. D. Powell and M. R. Horton ()
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R. W. Hallowell: Beth Israel Deaconess Medical Center, Harvard Medical School
S. L. Collins: Johns Hopkins University School of Medicine
J. M. Craig: Johns Hopkins Bloomberg School of Public Health
Y. Zhang: Shanghai Pulmonary Hospital, Tongji University School of Medicine
M. Oh: Johns Hopkins University School of Medicine
P. B. Illei: Johns Hopkins University School of Medicine
Y. Chan-Li: Johns Hopkins University School of Medicine
C. L. Vigeland: Johns Hopkins University School of Medicine
W. Mitzner: Bloomberg School of Public Health, Johns Hopkins University
A. L. Scott: Bloomberg School of Public Health, Johns Hopkins University
J. D. Powell: Johns Hopkins University School of Medicine
M. R. Horton: Johns Hopkins University School of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms14208

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