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

Author

Listed:
  • 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
    Institut National de la Santé et de la Recherche Médicale)

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.

Suggested Citation

  • 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 R, 2017. "Type-2 innate lymphoid cells control the development of atherosclerosis in mice," Nature Communications, Nature, vol. 8(1), pages 1-11, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15781
    DOI: 10.1038/ncomms15781
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