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PMI 126 - Lecture 16

PMI 126 - Lecture 16 - PMI 126 Lecture 16 TH-1 =>...

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PMI 126 Lecture 16 TH-1 => production of interferon gamma => directly involve in activation of NK, macrophage, and CTL. TH-2 => production of IL-4, IL-5, and IL-10 => focus its effort toward telling the B cell what specific antibody to make Cytotoxic T cells: affect the viral-infected cells CTL express CD8 on the surface - TCR recognizes the antigen peptide: MHC Class I on the surface of the target cell. - CD8 on CTL bind to MHC class I to stabilize the interaction - cell-adhesion molecules (LFA-1 and ICAM-1) help further interaction between target cell and Cytotoxic T cell. => result tight association between cytotoxic T cell and target cell => cytoskeleton and Golgi apparatus of CTL rearrange to face the target cells => granules within CTL release directly onto the target cell <= granules contain granzymes and perforin. <= perforin closely resemble the complement complex. - perforin makes pores on the surface of the target cell. - these pores allow the granzymes to get into the targtet cells - granzymes induce the target cells to undergo apoptosis through different pathways. - Target cells don’ t burst open to induce inflammatory response. 2 theories of perforin function: 1) Direct transport via pore formation of granzymes. 2) Binds to target cell membrane and gains access to endosome, transports granzyme out of endosome to cytosol. Granzymes interact directly with mitochondrion and result cytochorme C release. (Facilitate apoptosis) Another way that cytotoxic T cells kill other cells: through Fas pathway. - activated CTL has Fas ligand on the surface - Fas: Fas ligand interaction also induces apoptosis of the target cell.
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Viral Infection You might survive without adaptive immune system but you cannot survive without innate immune system. - viral-infected cells produce interferons - cells around the infected cells set up the anti- viral state upon the binding of interferons to the corresponding receptors - this SLOWS DOWN the viral infection even though interferons cannot clear the virus. What trigger NK cells => the absence of MHC class I on the target cell. As NK cells become infected, they produce IFN- gamma.
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