A commentary published in Cell Metabolism highlights research into low-grade adipose inflammation and its ability to trigger insulin resistance in individuals impacted by obesity. While the relationship between the two is well-documented, the precise mechanism by which such inflammation begins in those with obesity remains unclear. To shed light on the matter, the commentary cites a study co-authored by Dr. Willa Hsueh and published in Cell Metabolism as “Class II Major Histocompatibility Complex Plays an Essential Role in Obesity-Induced Adipose Inflammation.”
In the paper, Dr. Willa Hsueh and her peers discuss how adipose-resident T cells, or ART for short, mediate inflammation in people with obesity. The researchers emphasize several genes linked to MHCII antigen processing. The study looked at mice with obesity induced by a diet high in fat. The mice demonstrated an increase in adipocyte MHCII, which in turn tracked to increases in the ART markers indicative of inflammation.
The study concludes that the mouse model suggests a mechanism of action by which ART and MCHII promote adipose inflammation.
In the paper, Dr. Willa Hsueh and her peers discuss how adipose-resident T cells, or ART for short, mediate inflammation in people with obesity. The researchers emphasize several genes linked to MHCII antigen processing. The study looked at mice with obesity induced by a diet high in fat. The mice demonstrated an increase in adipocyte MHCII, which in turn tracked to increases in the ART markers indicative of inflammation.
The study concludes that the mouse model suggests a mechanism of action by which ART and MCHII promote adipose inflammation.