Lymphocytes in obesity-related adipose tissue inflammation

Diabetologia. 2012 Oct;55(10):2583-2592. doi: 10.1007/s00125-012-2607-0. Epub 2012 Jun 26.


Inflammation in the white adipose tissue (WAT) is considered a major player in the development of insulin resistance. The role of macrophages accumulating in the WAT during obesity, promoting WAT inflammation and insulin resistance is well established. In contrast, less is known about the role of lymphocytes. Recent studies have implicated different lymphocyte subsets in WAT inflammation. For instance, cytotoxic CD8(+) T cells infiltrating the WAT may contribute to the recruitment, differentiation and activation of macrophages. On the other hand, a differential role for CD4(+) Th1 and CD4(+) Th2 cells has been suggested. Levels of WAT regulatory T cells decrease during the course of obesity and may represent a crucial factor for the maintenance of insulin sensitivity. Moreover, activation of natural killer T cells, an innate-like T cell population, which recognises lipid antigens, promotes insulin resistance and WAT inflammation. Finally, B cells may infiltrate WAT very early in response to high-fat feeding and worsen glucose metabolism through modulation of T cells and the production of pathogenic antibodies. These interesting new findings however bear controversies and introduce novel, yet unanswered, questions. Here, we review and discuss the impact of the different lymphocyte subsets in obesity-related WAT inflammation and attempt to identify the open questions to be answered by future studies.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipose Tissue, White / pathology
  • Adipose Tissue, White / physiopathology*
  • Animals
  • B-Lymphocyte Subsets / physiology
  • Disease Models, Animal
  • Humans
  • Inflammation / pathology
  • Inflammation / physiopathology*
  • Leptin / physiology
  • Lymphocytes / physiology*
  • Mice
  • Obesity / pathology
  • Obesity / physiopathology*
  • T-Lymphocyte Subsets / physiology


  • Leptin