Macrophages, immunity, and metabolic disease

Immunity. 2014 Jul 17;41(1):36-48. doi: 10.1016/j.immuni.2014.05.010.

Abstract

Chronic, low-grade adipose tissue inflammation is a key etiological mechanism linking the increasing incidence of type 2 diabetes (T2D) and obesity. It is well recognized that the immune system and metabolism are highly integrated, and macrophages, in particular, have been identified as critical effector cells in the initiation of inflammation and insulin resistance. Recent advances have been made in the understanding of macrophage recruitment and retention to adipose tissue and the participation of other immune cell populations in the regulation of this inflammatory process. Here we discuss the pathophysiological link between macrophages, obesity, and insulin resistance, highlighting the dynamic immune cell regulation of adipose tissue inflammation. We also describe the mechanisms by which inflammation causes insulin resistance and the new therapeutic targets that have emerged.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adipose Tissue / cytology
  • Adipose Tissue / immunology*
  • Animals
  • Cytokines / immunology
  • Cytokines / metabolism
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / immunology*
  • Diabetes Mellitus, Type 2 / physiopathology
  • Humans
  • Inflammation / drug therapy
  • Inflammation / immunology
  • Insulin Resistance / immunology*
  • Liver / cytology
  • Liver / immunology
  • Macrophage Activation / immunology
  • Macrophages / immunology*
  • Mice
  • Muscle, Skeletal / cytology
  • Muscle, Skeletal / immunology
  • Obesity / drug therapy
  • Obesity / immunology*
  • Obesity / physiopathology
  • Signal Transduction / immunology

Substances

  • Cytokines