| First Author | Mehta P | Year | 2015 |
| Journal | J Leukoc Biol | Volume | 97 |
| Issue | 1 | Pages | 121-34 |
| PubMed ID | 25395302 | Mgi Jnum | J:216571 |
| Mgi Id | MGI:5609037 | Doi | 10.1189/jlb.3A0414-211RR |
| Citation | Mehta P, et al. (2015) gammadelta T cells promote inflammation and insulin resistance during high fat diet-induced obesity in mice. J Leukoc Biol 97(1):121-34 |
| abstractText | gammadelta T cells are resident in AT and increase during diet-induced obesity. Their possible contribution to the inflammatory response that accompanies diet-induced obesity was investigated in mice after a 5 to 10 week milk HFD. The HFD resulted in significant increases in CD44(hi), CD62L(lo), and TNF-alpha(+) gammadelta T cells in eAT of WT mice. Mice deficient in all gammadelta T cells (TCRdelta(-/-)) or only Vgamma4 and Vgamma6 subsets (Vgamma4/6(-/-)) were compared with WT mice with regard to proinflammatory cytokine production and macrophage accumulation in eAT. Obesity among these mouse strains did not differ, but obese TCRdelta(-/-) and Vgamma4/6(-/-) mice had significantly reduced eAT expression of F4/80, a macrophage marker, and inflammatory mediators CCL2 and IL-6 compared with WT mice. Obese TCRdelta(-/-) mice had significantly reduced CD11c(+) and TNF-alpha(+) macrophage accumulation in eAT after 5 and 10 weeks on the HFD, and obese Vgamma4/6(-/-) mice had significantly increased CD206(+) macrophages in eAT after 5 weeks on the diet and significantly reduced macrophages after 10 weeks. Obese TCRdelta(-/-) mice had significant reductions in systemic insulin resistance and inflammation in liver and skeletal muscle after longer-term HFD feeding (10 and 24 weeks). In vitro studies revealed that isolated gammadelta T cells directly stimulated RAW264.7 macrophage TNF-alpha expression but did not stimulate inflammatory mediator expression in 3T3-L1 adipocytes. These findings are consistent with a role for gammadelta T cells in the proinflammatory response that accompanies diet-induced obesity. |
