Combined B- and T-cell deficiency does not protect against obesity-induced glucose intolerance and inflammation

Cytokine. 2013 Apr;62(1):96-103. doi: 10.1016/j.cyto.2013.02.009. Epub 2013 Mar 9.


Obesity-induced inflammation is associated with insulin resistance and morphologically characterized by macrophage influx into the adipose tissue. Recently, various other immune cells, including B- and T-cells, have been shown to participate in modulating adipose tissue inflammation during the development of obesity. We show that HFD-feeding modulates the influx of B and T-cells into adipose tissue of obese animals, suggestive of a role of the adaptive immune system in the development of adipose tissue inflammation. Despite a lower bodyweight after HFD-feeding, gene expression levels of CD68, F4/80 and MCP-1 in white adipose tissue were enhanced in SCID animals that lack B- and T-cells. Moreover, conditioned medium from adipose tissue explants of HFD-fed SCID mice revealed increased release of IL-6 and CXCL1 compared to WT animals. Compared to WT mice, glucose tolerance was impaired in B- and T-cell deficient mice after HFD-feeding. Thus, complete B- and T-cell deficiency does not protect against HFD-induced adipose tissue inflammation and glucose intolerance. In contrast, SCID mice showed an increased pro-inflammatory status at the level of the adipose tissue in some cytokines. Our findings suggest that a delicate balance between various B- and T-cell populations controls adipose tissue inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism
  • Adipose Tissue / pathology
  • Animals
  • B-Lymphocytes / metabolism*
  • Body Weight
  • Diet, High-Fat
  • Epididymis / pathology
  • Feeding Behavior
  • Glucose Intolerance / complications*
  • Glucose Intolerance / pathology
  • Inflammation / complications*
  • Inflammation / pathology
  • Lymphocyte Depletion*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, SCID
  • Obesity / complications*
  • Obesity / prevention & control*
  • T-Lymphocytes / metabolism*