Type-2 innate lymphoid cells control the development of atherosclerosis in mice

Stephen A. Newland, Sarajo Mohanta, Marc Clément, Soraya Taleb, Jennifer A. Walker, Meritxell Nus, Andrew P. Sage, Changjun Yin, Desheng Hu, Lauren L. Kitt, Alison J. Finigan, Hans-Reimer Rodewald, Christoph J. Binder, Andrew N. J. McKenzie, Andreas J. Habenicht and Ziad Mallat ()
Additional contact information
Stephen A. Newland: University of Cambridge
Sarajo Mohanta: Institute for Cardiovascular Prevention, Ludwig-Maximilians-University (LMU)
Marc Clément: University of Cambridge
Soraya Taleb: Institut National de la Santé et de la Recherche Médicale
Jennifer A. Walker: MRC Laboratory of Molecular Biology
Meritxell Nus: University of Cambridge
Andrew P. Sage: University of Cambridge
Changjun Yin: Institute for Cardiovascular Prevention, Ludwig-Maximilians-University (LMU)
Desheng Hu: State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, Xiamen University
Lauren L. Kitt: University of Cambridge
Alison J. Finigan: University of Cambridge
Hans-Reimer Rodewald: German Cancer Research Center
Christoph J. Binder: Medical University of Vienna and Center for Molecular Medicine (CeMM) of the Austrian Academy of Sciences
Andrew N. J. McKenzie: MRC Laboratory of Molecular Biology
Andreas J. Habenicht: Institute for Cardiovascular Prevention, Ludwig-Maximilians-University (LMU)
Ziad Mallat: University of Cambridge

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

Abstract: Abstract Type-2 innate lymphoid cells (ILC2) are a prominent source of type II cytokines and are found constitutively at mucosal surfaces and in visceral adipose tissue. Despite their role in limiting obesity, how ILC2s respond to high fat feeding is poorly understood, and their direct influence on the development of atherosclerosis has not been explored. Here, we show that ILC2 are present in para-aortic adipose tissue and lymph nodes and display an inflammatory-like phenotype atypical of adipose resident ILC2. High fat feeding alters both the number of ILC2 and their type II cytokine production. Selective genetic ablation of ILC2 in Ldlr−/− mice accelerates the development of atherosclerosis, which is prevented by reconstitution with wild type but not Il5−/− or Il13−/− ILC2. We conclude that ILC2 represent a major innate cell source of IL-5 and IL-13 required for mounting atheroprotective immunity, which can be altered by high fat diet.

Date: 2017
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DOI: 10.1038/ncomms15781

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