Apr, 2022 - By WMR
Researchers found that modification of checkpoint proteins in the immune system regulates inflammation in fat tissue, which significantly reduces diabetes and obesity in pre-clinical model
Earlier research discovered that inflammation linked to obesity causes more comorbidities, however, the mechanisms that are responsible for this inflammation are still unclear. Now, a group of researchers at University Hospital Erlangen, Germany and Trinity College Dublin, Ireland discovered a new mechanism in which modification of checkpoint proteins in the immune system regulates inflammation in fat tissue significantly reducing obesity and diabetes in pre-clinical mode.
The new research involved a protein named programmed death-ligand 1 (PD-L1), which helps regulating immune response of body. PD-L1 can form bond with receptors on T-cells further preventing these deadly immune cells from killing cells containing PD-L1 molecule, which could include cancer cells. The team investigated the role of PD-L1 in regulation of immune system linked to obesity and the mechanism by which it causes inflammation in fat tissue. The team conducted experiments on mice and demonstrated that modification of the PD-L1 protein on specific immune cells changed the inflammatory cells present in the fat tissue.
After modifying the protein in mouse models with obesity that were given high-fat diet, the team observed the development of obesity as well as diabetes significantly reduced. By analyzing sample of humans with obesity, the scientists also demonstrated that the changed expression of checkpoint proteins was liked with weight of the person. With the discovery of this mechanism, with more work new treatment for obesity can be developed and with these new ways to manage the conditions, the lethal side effects of obesity such as cancer, diabetes, and cardiovascular disorders could also be managed.
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