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10 Cards in this Set
- Front
- Back
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what is the danger theory model
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the immune system detects danger signals from injured cells and activates the immune system. APC's detect mechanical damage, components of injured cells, pathogens, toxins, immuno stimulatory compounds, cytokines, this releases mediators that activate the innate system producing inflammation
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what is necrosis, reversible vs non-reversible injury
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necrosis is the passive catabolic death of a cell
Reversible injury: – swelling of the cell and its organelles – blebbing of the plasma membrane – clumping of nuclear chromatin Irreversible injury: swelling and disruption of lysosomes swelling mitochondria disruption of cellular membranes profound nuclear changes: condensation (pyknosis) fragmentation (karyorrhexis) dissolution of the nucleus (karyolysis). |
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what are the necrosis danger signals
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HMGB1, High mobility group box
1, is a protein passively released during necrosis. – Activates NF-κB pathway – RAGE is receptor for HMGB1. • Uric acid is another diffusible danger signal: – Activates NF-κB pathway • HSPs are another danger signals. – HSPs induce NF-κB pathway and release of inflammatory cytokines (TNF-α and IL-1β). |
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what are the steps to danger response
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increase in blood supply to area, redness and heat, increased permeability of capillaries (swelling and pain), massive influx of neutrophils, influx of macrophages (16-48hrs)
MΦ-mediated phagocytosis of debris, restoring the homeostasis |
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what is the humoral response to danger signals
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Soluble inflammatory mediators:
• Complement • Cytokines • Chemokines, other mediators • Leucotrienes and Prostaglandins • Reactive oxygen intermediates and nitric oxide |
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how do wounds heal
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Tissue repair and remodeling involves the development of new blood vessels
(angiogenesis), resurfacing of the wound (re-epithelialization) and collagen deposition (fibroblasts) |
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What happens to the immune system during apoptosis
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there is no immune response, apoptosis can render APCs into an immuno suppression
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what are the steps of apoptosis
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trigger:
DNA damage Cytokine starvation Hypoxia Temperature Death receptor regulators: Death domain factors Cytochrome c p53 Bcl-2 family Myc/oncogenes executioners: caspases |
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what are caspases
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they are proteases that exist as latent precursors.
• When activated, caspases initiate apoptosis by destroying key components of the cellular infrastructure. |
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what are the two apoptitic pathways
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(intrensic) 3 main triggers of apoptosis:
1. Bcl-2 protein 2. Calcium 3. Free radicals extrensic-- Extracellular signals may include toxins[9], hormones, growth factors, nitric oxide[10] or cytokines, and therefore must either cross the plasma membrane or transduce to effect a response Fas (CD95) is cell death receptor. FasL (Fas ligand, CD95L) is a transmembrane protein of the tumor necrosis factor (TNF) family. FADD – Fas Associated Protein with Death Domain DISC – death-inducing signaling complex |
