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Natural Killer Cells

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The cytotoxicity of natural killer cells is a topic that is still being investigated today, specifically the question at hand is “How does a cytotoxic T cell (or NK cell) avoid being killed by the perforin and granzymes that it secretes to kill a target cell?”
In the field, what is known about the topic includes the function of these natural killer cells, the mechanism of action of the perforin released by these cells, and health issues associated with nonfunctional perforin. Natural killer cells are a type of white blood cells that play significant roles in viral infections and host-rejection of tumors and are cytotoxic because they contain perforin and granzymes. When cytotoxic T lymphocytes and natural killer cells are activated, they produce …show more content…
Perforin is a glycoprotein responsible for the formation of pores in the cell membranes of target cells and is found in the granules of cytotoxic T lymphocytes and natural killer cells. Perforin binds to the target cells through the phospholipids on the cell membrane. Perforin polymerizes with the help of calcium ions to form transmembrane channels. The formation of these pores disrupts the cell membrane while allowing for the passive diffusion of pro-apoptotic proteases, granzymes, into the target cell leading to cell death. Before perforin is released, the cells that produce is transported it from the endoplasmic reticulum to the Golgi and into the secretory granules where it is packaged together with granzymes. The secretory granules fuse with the plasma membrane of the cytotoxic cell and allow its release into the junctions between the immune cell and the cell it aims to kill. Infants born without functional perforin develop familial hemophagocytic lymphohistiocytosis (FHL), which is an aggressive immunoregulatory …show more content…
Type 1 interferon is a group of interferon proteins that help regulate the activity of the immune system, which plays a crucial role in antiviral defense. Results indicate that after viral infection, natural killer cells lacking IFNAR or STAT1 malfunction in expansion and memory cell formation. These cells showed increased apoptosis despite comparable proliferation when compared to the wild-type NK cells. Results also showed that type I IFN acts to combat NK cell–mediated fratricide that is dependent on NKG2D (receptors that play and important role in host protection) triggering and perforin release during viral infection. Through an adoptive transfer of IFNAR lacking NK cells into NK cell deficient mice, the NK cell can generate a cell memory during infection in hosts lacking wild-type NK cells. For this study, mouse strains of viral infections were used as well as Fluorescent labeled inhibitor of caspases, which measures activate caspases, as an indicator of

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