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Hepatoma Fas - FasL pathway immune escape mechanisms and countermeasures
PAGE \* MERGEFORMAT 18
Hepatoma Fas / FasL pathway immune escape mechanisms and countermeasures
[Keywords] expression of Fas, FasL in · cell apoptosis in liver tumors · immune
Fas is a cell surface death receptors, signaling molecules of apoptosis expression of Fas and its ligand FasL binding, activation and conduction of apoptosis signal, an important way to induce apoptosis of tumor occurrence and development of apoptosis exceptions are closely related, in which the tumor cells resistant to Fas-mediated apoptosis and counterattack immune cells to the T-cell apoptosis, is an important mechanism of immune evasion of tumor cells through Fas / FasL system in recent years, domestic and foreign scholars on the relationship of the Fas / FasL system and liver cancer immune escape mechanisms and their corresponding countermeasures conducted in-depth research and study, now in the field of research reviewed in the paper.
Fas / of FasL system and apoptosis induced by
Fas and FasL interaction is an important way to induce apoptosis and Fas also the said Apo1 or CD95, belongs to the tumor necrosis factor receptor (TNFR / nerve growth factor receptor (NGFR OF NEURONS family type Ⅰ transmembrane glycoprotein Fas antigen mainly in the form of a membrane receptor, but also through different splicing at the transcriptional level of mRNA translation product missing transmembrane region of the formation of soluble Fas (of sFas and present in the cytoplasm and serum of sFas ligand FasL combination, can be blocked by FasL and membrane receptor Fas apoptosis since inhibition compared with the corresponding cells, tumor cells are usually of Fas expression is low or completely expressed, but there are also malignant transformation of cells emerging after the expression of Fas.
FasL is a natural ligand of Fas in the human body is a type II transmembrane protein belonging to the TNF family, FasL was mainly expressed in activated T cells, NK cells, some tumor cells and s
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