ABSTRACT
Platelets are small anucleated fragments derived from megakaryocytes participating in coagulation and hemostasis. In recent years, more and more experimental and clinical evidences show that platelets also promote tumor metastasis. When tumor cells detach from the primary tumor and access the blood, platelets are the first host cells they encounter. As an important member of tumor metastasis microenvironment, platelets and tumor cells interact and affect each other. On the one hand, tumor cells can regulate the function of platelets by inducing platelets activation and aggregation; on the other hand, platelets can promote tumor metastasis by directly contacting and releasing bioactive mediators. Numerous studies have shown that platelets can promote tumor metastasis through the following approaches: 1. Reducing the shear force-induced damage; 2. Helping tumor cells escape immune surveillance; 3. Promoting tumor cells migration and stationary adhesion in blood vessels; 4. Promoting epithelial-mesenchymal transition of tumor cells; 5. Promoting tumor cell extravasation; 6. Forming a metastatic niche suitable for the survival of tumor cells. Therefore, targeting the interaction between platelets and tumor cells has become a potential tumor treatment strategy. Based on the latest research progress at home and abroad, this paper reviews the roles of platelets in different stages of tumor metastasis and the application of antiplatelet drugs in tumor therapy.
ABSTRACT
B / T lymphuocyte attenuator (BTLA) is one of the important checkpoint molecules in immune regulation. BTLA belongs to the CD28 superfamily, and its protein structure is similar to programmed cell death-1 (PD-1) and cytotoxic T lymphocyte associated antigen-4 (CTLA-4). BTLA is mainly expressed in B and T cells, and has also been found in some innate immune cells such as dendritic cells and monocytes. To date, the herpesvirus entry mediator (HVEM) is the only ligand for BTLA found in human cells. HVEM belongs to the Tumor necrosis factor receptor (TNFR) superfamily, and its interaction with BTLA directly connects CD28 and TNFR families. The binding of BTLA with HVEM often mediates immunosuppressive effects and plays an important role in maintaining immune tolerance. However, recent studies have found that the BTLA / HVEM pathway not only provides negative regulatory signals, but also promotes the survival of T cells. This bidirectional signaling system renders BTLA-mediated immune regulation more sophisticated and complex. Growing evidence has shown that BTLA is involved in T cells, B cells and dendritic cell-mediated immune regulation, and therefore plays an important role in a variety of immune related diseases, such as inflammation, tumor, infectious diseases and autoimmune diseases. Based on the latest research progress at home and abroad, this paper reviews the role of BTLA in immune regulation and immune related diseases.