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Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226

With abundant research on group 2 innate lymphoid cells (ILC2s) published over the years, ILC2s are widely known to be implicated in regulating various ...

Fourth Military Medical University

Mounting evidence suggests that platelets play an essential role in cancer metastasis. The interactions between platelets and circulating tumor cells (CTCs) promote cancer metastasis. CTCs induce platelet activation and aggregation, and activated platelets gather and protect CTCs from shear stress and natural killer cells. Finally, platelets stimulate CTC anoikis resistance, epithelial-to-mesenchymal transition, angiogenesis, extravasation, and eventually, metastasis. Cell adhesion molecules (CAMs) have been identified as active players during the interaction of CTCs with platelets, but the specific mechanism underlying the contribution of platelet-associated CAMs to CTC metastasis remains unclear. In this review, we introduce the mechanism of platelet-related tumor metastasis and particularly focus on the role of CAMs in it.

Platelet-mediated tumor metastasis mechanism and the role of cell adhesion molecules.

Obesity is associated with chronic low-grade inflammation, contributing to an increasing prevalence of chronic metabolic diseases, such as insulin resistance, non-alcoholic fatty liver disease (NALFD), and steatohepatitis. Macrophages are the predominant immune cells in adipose tissues. Adipose tissue macrophages (ATMs) would switch to pro-inflammatory M1 state during obesity, causing local and systemic inflammation. However, the regulatory mechanism of ATMs has not yet been well described within this process. Using a high-fat diet (HFD)-induced mouse obesity model, we found that the costimulatory molecule CD226 was highly expressed on ATMs and knockout (KO) of CD226 alleviated obesity caused by HFD. Loss of CD226 reduced the accumulation of ATMs and hindered macrophage M1 polarization, with lower serum proinflammatory cytokine levels. Furthermore, deficiency of CD226 on ATMs decreased the phosphorylation levels of VAV1, AKT, and FOXO1 and thereby upregulated PPAR-γ. Further administration of PPAR-γ inhibitor restored M1 phenotype in CD226KO ATMs. In summary, loss of CD226 alleviates the HFD-induced obesity and systemic inflammation through inhibition of the accumulation and M1 polarization of ATMs in which PPAR-γ-dependent signaling pathway is involved, suggesting that CD226 may be identified as a potential molecular target for the clinical treatment of obesity.

Yitian Liu

Orthopedic Department of Tangdu Hospital

Fourth Military Medical University

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226

Yitian Liu

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Orthopedic Department of Tangdu Hospital

Fourth Military Medical University

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226

Orthopedic Department of Tangdu Hospital