PD-L1 can improve diet induced obesity From The latest research on the sub Journal of Science

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Obesity has become a major health problem for many people, and obesity is closely related to many other diseases.

Previous studies have shown that obesity related inflammation can lead to comorbidity, and immune regulation plays an important role in adipose tissue homeostasis. There is increasing evidence that the immune system of obese patients is seriously dysregulated and leads to mild inflammation. Immune cells play an important role in the stability of the internal environment of adipose tissue. The imbalance between pro-inflammatory cells and anti-inflammatory cells will promote the progress of obesity. However, how does the non-inflammatory homeostatic environment change into an inflammatory state leading to obesity? The starting mechanism of this series of processes is not clear.

Programmed death ligand 1 (PD-L1) is one of the key molecules regulating adaptive immunity. PD-L1 has been proved to be an effective regulator of T cell polarization. It has been found that macrophages, dendritic cells and type 2 innate lymphocytes (ilc2) express PD-L1 and regulate PD-1-expressing T cells and ilc2. Antibody mediated PD-L1 inhibits the release of Th1 cells in antitumor and autoimmune responses. Therefore, we hypothesized that PD-L1 plays an important role in maintaining environmental stability in adipose tissue, and studied the cell-specific function of PD-L1 during obesity using transgenic mice in diet induced obesity model and obese patient samples.

Recently, the professional academic journal scientific translational medicine recently published a study on obesity. Researchers from Germany and Ireland used conditional gene knockout mice to study the role of costimulatory molecule PD-L1 in diet induced obesity.

The researchers found that PD-L1 on dendritic cells can control the adaptive immune response in adipose tissue, thereby limiting diet induced obesity. In mice on a high-fat diet, dendritic cell PD-L1 deficiency promoted increased obesity and impaired adipose tissue T cell polarization. However, anti-PD-L1 mAb treatment reduced glucose tolerance in mice on a high-fat diet. The expression of PD-L1 in adipose tissue of obese patients also increased, suggesting that PD-L1 on dendritic cells may also fight human fat inflammation.

During diet induced obesity, PD-L1 functional ablation of dendritic cells using conditional gene knockout mice can increase body weight and produce metabolic syndrome, while PD-L1 expression on type 2 innate lymphocytes, T cells and macrophages is not necessary for obesity control.

Through co culture in vitro, dendritic cells interact with T cells and ilc2 through PD-L1: PD-1 axis to inhibit helper T cell type 1 Proliferation and promote type 2 polarization, respectively. The study also proved the role of PD-L1 in the regulation of human adipose tissue. The expression of PD-L1 in visceral fat of obese patients was positively correlated with weight gain. Therefore, the researchers defined the mechanism of adipose tissue homeostasis controlled by dendritic cell expression of PD-L1, which may be a clinically relevant finding of immune related adverse events during immune checkpoint inhibitor treatment.

Note: in vitro, dendritic cells interact with CD4 + T cells and ilc2 through the interaction of PD-L1: PD-1.

In the mouse model, PD-L1 expressed on dendritic cells plays an important role as an effective regulator of adipose tissue immunity: firstly, adipose tissue dendritic cells express a large amount of PD-L1 in mice and humans; Second, the lack of structural PD-L1 and dendritic cell specific PD-L1 will lead to weight gain, damage metabolic function, and transfer T cell polarization to Th1; Finally, PD-L1 blockade in vitro affects Th2 polarization and ilc2 function. Combined with the results of checkpoint inhibition in vivo in this study, the researchers found their direct effects on T cell polarization and weight loss. These data show that PD-L1 on dendritic cells maintains the steady-state environment of adipose tissue and can fight inflammation.

In conclusion, based on the previous findings, the results of this new study confirmed that anti-PD-L1 monoclonal antibody treatment reduced glucose tolerance in mice on high-fat diet, and pointed out the potential role of PD-L1 on dendritic cells against human fat inflammation.

Reference source:

1. Schwartz C, Schmidt V, Deinzer A, Hawerkamp HC, Hams E, Bayerlein J, Röger O, Bailer M, Krautz C, El Gendy A, Elshafei M, Heneghan HM, Hogan AE, O’Shea D, Fallon PG. Innate PD-L1 limits T cell-mediated adipose tissue inflammation and ameliorates diet-induced obesity. Sci Transl Med. 2022 Mar 9;14(635):eabj6879.

doi: 10.1126/scitranslmed.abj6879. Epub 2022 Mar 9. PMID: 35263149.

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