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Cell Rep. 2019 Jul 2;28(1):202-217.e7. doi: 10.1016/j.celrep.2019.06.016.

Innate Lymphoid Cells in the Induction of Obesity.

Author information

1
Laboratory for Innate Immune Systems, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan; Laboratory for Immune Cell Systems, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan; Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan.
2
Laboratory for Innate Immune Systems, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan; Department of Medical Life Science, Graduate School of Medical Life Science, Yokohama City University, Kanagawa, Japan; Laboratory for Innate Immune Systems, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Osaka, Japan. Electronic address: kazuyo.moro@riken.jp.
3
Laboratory for Metabolic Homeostasis, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan.
4
Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan; Department of Medical Life Science, Graduate School of Medical Life Science, Yokohama City University, Kanagawa, Japan.
5
Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan; Department of Medical Life Science, Graduate School of Medical Life Science, Yokohama City University, Kanagawa, Japan; Intestinal Microbiota Project, Kanagawa Institute of Industrial Science and Technology, Kanagawa, Japan.
6
Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
7
Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.
8
Laboratory for Immune Cell Systems, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan; Deparment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan. Electronic address: shigeo.koyasu@riken.jp.

Abstract

Complex interactions between immune cells are an important component in the induction of obesity. Here, we show that Il2rg-/-Rag2-/- mice lacking all lymphocytes are resistant to diet-induced obesity. Transplantation of bone marrow cells from Rag2-/- mice, which lack only acquired immune cells, into Il2rg-/-Rag2-/- mice abolishes this resistance, indicating a role for innate lymphoid cells (ILCs) in this process. Mice lacking ILC2 or ILC3 cells, but not natural killer cells, are resistant to obesity. Adoptive transfer of naive ILC2s isolated from the small intestine (SI), but not ILC2s from white adipose tissue (WAT), restores the induction of diet-induced obesity in Il2rg-/-Rag2-/- mice. Analysis of transcriptional differences reveals that SI-ILC2s express higher levels of IL-2 than do WAT-ILC2s and that blockade of IL-2 signaling impairs weight gain and reduces the populations of ILC2s and ILC3s in the SI, suggesting a role for the IL-2/ILC2/3 axis in the induction of obesity.

KEYWORDS:

ILC2; ILC3; common gamma chain; high-fat diet; innate lymphoid cells; interleukin-2; obesity; small intestine; white adipose tissue; γ(c)

PMID:
31269440
DOI:
10.1016/j.celrep.2019.06.016
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