Research continues to reveal the role that inflammation plays in obesity and the development of comorbidities, and new research sheds even more light on the problem. Scientists have found that modification of so-called “checkpoint proteins” in the immune system can regulate adipose tissue inflammation, resulting in significantly reduced obesity and diabetes in preclinical models.
The breakthrough was made by scientists from the University Hospital of Germany in Erlangen and the Irish Trinity College in Dublin and includes a protein called programmed death ligand 1, or PD-L1. This protein acts as a type of “brake” that helps regulate the body’s immune response, and for this reason it has come to play an important role in cancer immunotherapy.
PD-L1 has the ability to bind to receptors on important T cells, preventing these immune killer cells from selecting dangerous cells that contain the PD-L1 molecule, which may include cancer cells. Anticancer drugs called checkpoint inhibitors designed to bind to PD-L1 and block this action, in turn releasing the brakes and allowing the killer T cells to begin work.
The authors of this new study sought to learn more about the role of PD-L1 in regulating the immune system with respect to obesity and how it causes inflammation of the adipose tissue that causes the condition. Through experiments on mice, scientists were able for the first time to show how modification of the PD-L1 protein on key immune cells alters inflammatory cells in adipose tissue.
The result of these adjustments in mouse models of diet-induced obesity fed a high-fat Western-style diet resulted in a dramatic reduction in the development of obesity and diabetes. By analyzing samples of obese people, the team was also able to show that these changes in protein expression checkpoints correlated with human weight.
“In our study, we analyzed the function of immune checkpoints on specific cells, and it is interesting to see that a small change in one of the many cell populations in fat so affects disease outcome,” said study author Dr. Christian Schwartz.
By discovering this mechanism, scientists hope that with further research they will be able to develop new ways to combat obesity and its harmful effects, such as diabetes, cancer and cardiovascular disease.
“Only through our baseline research efforts using preclinical models have we been able to access patient samples and link our findings to human disease,” Schwartz said. “It will be interesting to explore how we can manipulate this checkpoint on specific cell populations of interest to help obese people.”
The study is published in the journal Science Translational Medicine.
Source: Trinity College London via EurekAlert
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