γδ T Cells and diet-induced inflammation in adipose tissue (173.2)

Abstract

Abstract Adipose tissues contain several subsets of immune cells. Relatively little is known about their contributions to adipose tissue inflammation induced by feeding mice a diet rich in saturated fats. Using a model of diet-induced obesity in male C57BL/6J mice, we investigated the possible contributions of γδ T cells to this inflammation. γδ T cells make up about one-third of the total T cell population in the epididymal adipose tissue. The γδ T cell receptor was blocked in wild-type mice using an anti-TCRδ antibody. A decrease in macrophage marker F4/80 was observed in these mice as compared to saline-treated control mice on high fat diet (HFD). TCRδ-/- mice adipose tissue failed to show an increase in mRNA expression of cytokines such as CCL-2, IL-6, IFN- γ even though they ate similar amounts of food and showed similar weight gain pattern as wild-type mice. A fraction of adipose tissue γδ T cells were shown to produce IFN-γ in obese mice by flow cytometry and were CD27+, a marker for IFN-γ-producing γδ T cells in the periphery. Obesity also results in inflammation in the skeletal muscle and liver, along with adipose tissue inflammation. Obese TCRδ-/- mice have reduced expression of markers of inflammation in the muscle after 5 weeks on HFD and liver after 6 months on HFD as compared to wild-type mice. These results are consistent with the conclusion that adipose tissue, liver and skeletal muscle inflammation during high saturated fat feeding is dependent in part on γδ T cells.