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26 Cards in this Set
- Front
- Back
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NK cells are impt. in innate immune system because they produce?
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IFN- gamma
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How are NK Cells activated?
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need to be activated to kill infected host cell:through two receptors both working.
The Activating Receptor and the Inhibitory receptor the activating receptor: needs to bind the NK cell ligand on the normal analogous cell and the inhibitory receptor bind nothing. |
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What does activation of NK lead to?
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degranulation which kills the infected cell - releases granules on target cell and it kills the target cell
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Why would NK cells be good at killing virally infected cells and tumor cells?
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because tumor cells have low expression of MHC thus, inhibitory receptor won't be activated and the cell will be killed.
virally infected cells won't have the 'self peptide' and thus, they will be killed as well. |
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So, we've got NK of the innate doing some killing what about the lymphocytes of the adaptive immune system?
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antigen specific cytotoxic T cell (ie: Cd8+ T cells) are involved with eradicating intracellular pathogens
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T/F Interactions with APC in LN are necessary to activate the T cells.
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true
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Do T cells leave the lymphnodes and go directly to the correct site of infection?
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no, they float throughout everywhere and then 'stick' to the area that has the right pathogen they are looking for.
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When CTLs get to the infection site, what are they killing?
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CTLs kill targets that express the same class I-associated antigen that triggered the proliferation and differentiation of naive CD8+ T cells to become CTLs
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How is the T Cell 'even more activated' once it reaches it's target cell?
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the target cell is expressing the MCHI/peptide complex and once the CTL cell binds, accessory molecules help to induce lots of activation and signal transduction. -
T cells then produce more granules and organize them towards target cell to prepare for release to kill target. |
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What is the main diff. between NK cells and CTL cells?
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NK cells aren't specific but CTLs are.
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Why are all of the signal transduction and cytokines leading the granules to the area of where the CTL is bound to the target so impt?
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because you want to release it to only kill the target and not everything surrounding it.
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How quickly does degranulation occur and kill the target?
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VERY quickly - within a few min.
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What are the main steps in CTL-mediated lysis of target cells?
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1. antigen recognition and conjugate formation
2. CTL activation 3. Granule exocytosis 4. Detachment of CTL 5. Target cell death |
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But, how does CTL lyse the target cell? What 2 ways did Dr. Bailey describe?
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**It uses the SAME mechanism as the NK cells!
Granule exocytosis -> entry of granzymes -> activation of caspases -> apoptosis of target cell ~ Release of granzyme/perforin complexes and endocytosed by target cell and granzymes enter cytoplasm via perforin dependent mechanisms (granzyme B NEEDS perforin to get into cell - via pores = most common route used) -> activation of apoptotic pathways |
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How does Granzyme B induce apoptosis?
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By activating CAPSPASES (specifically caspase 3)
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*After Granzyme B has activated Caspase what occurs?
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caspase 3 activation will lead to caspase activated DNAs (CAD)
CAD causes DNA fragmentation and thus = apoptosis |
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*Can Granzyme B DIRECTLY activate CAD?
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yes,
Granzyme B can also directly activate CAD |
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*T/F Can Granzyme B also activate sequence of molecules to eventually put pores in lipid membrane of mitochondria?
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YES, this liberates *CYTOCHROME C, which will induce apoptosis via *caspase 9 and *endonuclease G which cleaves DNA = apoptosis
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What is the more T Cell specific way of inducing apoptosis (NK don't do it)
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target cell and CTL are going to interact through Fas:FasL = apoptosis
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How do Fas:FasL interaction eradicate cells infected with an intracellular pathogen?
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On the Fas there are "death domains" that lead to signaling cascades that activate caspase 8 - that can activate BID...which leads to the Cytochrome C pathway = apoptosis
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What activates the death domain on Fas?
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Fas receptor trimerization activates the death domain - has to be 3 of them!
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T/F Fas ligand on the CTL activates Fas on target cell
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tre
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What specifically does the FADD (deathdomain) activate?
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caspase 8
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What does Caspase 8 activate?
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BID -> cytochrome C -> caspase 9 / endonuclease -> DNA fragmentation ->apoptosis
or (can activate caspase 3->DNAse) |
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How do intracellular pathogens (viruses, because these are mainly specialized for viruses) try to thwart the immune response?
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They play with antigen presentation
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Dr. Bailey's example questions:
**Which of the following ways does virus inhibit activation of T cell... inhibit activation of proteasome? Block Transport of protein to ER Block MHC synthesis Removal of Class I MHC from ER Interference with CTL recognition by "decoy" viral class I - like molecules: murine CMV ARE THE VIRUSES STILL SUSCEPTIBLE TO NK CELLS? |
ALL of the above!
yes, they are still susceptible to NK cells |
