Term
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Definition
| Cytotoxic effector CD8 T-cells that eliminate infected cells |
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Term
| What is the job of CD4 TH1-cells? |
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Definition
| Activation of macrophages so they can efficiently phagocytize intracellular pathogens |
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Term
| What can cause type IV hypersensitivity reactions? |
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Definition
| Proteins leading to local skin swelling cause delayed type; haptens or metal ions leading to local epidermal reaction cause type due to contact |
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Term
| What do effector CTL-cells do? |
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Definition
| They have altered levels of adhesion molecules (low L-selectin) which prevents movement into lymph nodes. They enter infected cells via VLA-4 binding to VCAM, causing increased CD2 and LFA-1 leading to cellular interactions |
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Term
| What is required for CD8 T cell activation? |
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Definition
| Help from CD4 TH1-cells, which increase levels of B7 on the APC via CD40L as well as produce paracrine IL-1. |
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Term
| What do active CTL-cells produce? |
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Definition
| IL-2 and high-affinity IL-2 receptors |
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Term
| What mediates the exocytic pathway of killing? |
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Definition
| Granzymes, perforin, and granulysin (cytotoxins) released after CTL-cells rearrange cellular machinery following TCR recognition. |
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Term
| Where do granzymes, perforin, and granulysin act? |
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Definition
| Lytic granules containing cytotoxins are released into the target cell membrane. Perforin and serglycin create pores into which granzyme-B can enter the cell |
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Term
| What signals are required for CTL-cells? |
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Definition
| Cell-cell contact at HLA class I, no second signal |
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Term
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Definition
| DNA is fragmented, nucleus is condensed, and plasma membrane forms vesicles for easy phagocytosis without inflammation |
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Term
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Definition
| Metabolic insults leads to leakage of cellular contents, yielding inflammation and monocyte recruitment |
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Term
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Definition
| Cysteine proteases that cleave proteins at aspartate residues, do not cleave DNA |
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Term
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Definition
| A caspase activatable DNA-ase found in the cytoplasm of all cells but is inhibited |
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Term
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Definition
| When activated by granzyme-B, it cleaves the inhibitor (I-CAD) to activate CAD. It also inhibits cellular integrity proteins (lamin B) and nuclear repair enzymes (PARP) and activates endonucleases |
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Term
| How do CTL-cells force death? |
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Definition
| Via "death receptors"--TNF family ligands and transmembrane receptors. |
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Term
| What is the FasL-Fas death pathway? |
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Definition
| Fas and FasL become expressed on activated T cells. Binding of FasL (3 molecules) to Fas initiates an apoptotic pathway: Fas and TNFR1 have "death domain" (DD) which recruits FADD to activate caspases |
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Term
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Definition
| Many cells, especially activated T-cells, some B-cells, but no naive lymphocytes |
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Term
| What mediates extrinsic programmed cell death? |
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Definition
| Granule exocytosis and death receptors. |
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Term
| What can cause intrinsic programmed cell death? |
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Definition
| UV exposure, chemotherapy drugs, starvation, or irreparable genetic damage |
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Term
| How does programmed cell death (PCD) occur? |
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Definition
| Mitochondria are told to release cytochrome c, which binds to Apaf-1 in the cytoplasm, activates cas-9, which activates cas-3 and the caspase chain is initiated |
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Term
| What regulates apoptosis? |
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Definition
| Molecules that promote apoptosis or enhance survival |
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Term
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Definition
| A pro-life molecule that prevents mitochondrial pore formation |
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Term
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Definition
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Term
| What is a hallmark of cancer? |
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Definition
| Ability to evade apoptosis |
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Term
| How is Bcl related to cancer? |
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Definition
| Overproduction of Bcl is seen in B-cell lymphomas |
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