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Questions and Answers
What is the primary function of ULBP1–3, MICA, and MICB proteins in relation to NK cells?
What is the primary function of ULBP1–3, MICA, and MICB proteins in relation to NK cells?
What types of cells primarily upregulate ULBP1–3, MICA, and MICB?
What types of cells primarily upregulate ULBP1–3, MICA, and MICB?
How does the balance of inhibitory and activating signals influence NK cell activity?
How does the balance of inhibitory and activating signals influence NK cell activity?
Which receptor on NK cells interacts with ULBP1–3, MICA, and MICB?
Which receptor on NK cells interacts with ULBP1–3, MICA, and MICB?
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In which scenario is NK cell activation most likely to occur?
In which scenario is NK cell activation most likely to occur?
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What role does perforin play in the process of apoptosis induced by Fas ligand and TNF?
What role does perforin play in the process of apoptosis induced by Fas ligand and TNF?
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Which molecules are primarily released to facilitate apoptosis through a pore-forming mechanism?
Which molecules are primarily released to facilitate apoptosis through a pore-forming mechanism?
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What is the primary consequence of granule release containing perforin and granzymes in target cells?
What is the primary consequence of granule release containing perforin and granzymes in target cells?
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What is necessary for granzymes to access the cytosol of a target cell?
What is necessary for granzymes to access the cytosol of a target cell?
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Which of the following statements about TNF and Fas ligand is true in the context of apoptosis?
Which of the following statements about TNF and Fas ligand is true in the context of apoptosis?
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Study Notes
NK Cell Activation
- Stressed cells, like those infected with viruses or cancerous cells, upregulate molecules like ULBP1-3, MICA, and MICB.
- These molecules are ligands for NKG2D receptors found on natural killer (NK) cells.
- Binding of these ligands to NKG2D triggers NK cell activation.
- NK cell activation depends on a balance between activating and inhibitory signals.
- Activating signals come from NKG2D binding, while inhibitory signals come from MHC class I molecules expressed on target cells.
NK Cell Cytotoxicity Mechanisms
- Activated NK cells induce apoptosis in the target cell.
- NK cells release cytotoxic granules containing perforin and granzymes.
- Perforin creates pores in the target cell membrane.
- Granzymes are then able to enter the cytosol and trigger apoptosis.
Resistance to Cell-Mediated Cytotoxicity
- Degranulation: Some cells have mechanisms to resist NK cell cytotoxicity.
- Cathepsin B: During degranulation, a protease called cathepsin B may cleave perforin, preventing pore formation.
- cFLIP Protein: NK cells express a protein called cFLIP that inhibits the caspase 8 pathway, which is a key pathway in apoptosis.
- Protease Inhibitor-8: NK cells also express protease inhibitor 8 (PI-8), which inhibits the activity of granzyme B.
- HLA-C, -E, and -G: Certain cells express specific MHC class I molecules like HLA-C, HLA-E, and HLA-G which can inhibit NK cell activation.
Phagocytosis by Macrophages
- After the target cell undergoes apoptosis, it is engulfed by macrophages, which are specialized immune cells that act as "big eaters."
- This process, called phagocytosis, removes cellular debris and further prevents infection spread.
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Description
This quiz explores the mechanisms of NK cell activation and their cytotoxic actions against stressed or infected cells. It delves into the balance of activating and inhibitory signals and the processes involved in inducing apoptosis in target cells. Test your knowledge on how NK cells recognize and kill abnormal cells!