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Innate Immunity (Cellular Defences (Neutrophils (Phagocytosis, Form of…
Innate Immunity
Cellular Defences
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Natural Killer cells
Monitor the expression of MHC 1 on cells. Virus-infected cells express less MHC 1 --> inhibition of the NK cell is lost + cell is displaying distress markers that the NK cell recognises --> release of perforin (forms pores) and granzymes (induce apoptosis by damaging mitochondria)
Innate source of IFN-gamma --> additional activation of macrophages and upregulation of their antimicrobial effector mechanisms
Recognition of PAMPs by PRRs on macrophages induces a cytoskeletal change in the macrophage, triggering ingestion of the pathogen
Neutrophils
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Form of programmed cell death in which they release chromatin and DNA that forms extracellular webs that trap pathogens
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Activation of TLRs in innate immune cells --> activation of NFkB and IFN pathways --> production of pro-inflammatory cytokines that recruit more immune cells and have systemic effects
Activation of NOD-receptors --> inflamasome activation --> activation of pro-inflammatory caspases --> pyrpoptosis (pro-inflammatory, programmed cell death) --> release of IL-1Beta and IL-18
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Basophils
Release a lot of histamine, ROSs
Barriers
Physical
Skin
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Outer layer of dead, dried cells that are hard for pathogens to get through
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Molecular Defences
Complement cascade
Secreted PRRs eg MBL (mannose binding lectin) bind directly to PAMPs on pathogen surface to trigger the complement cascade
C3a works on endothelial cells and mast cells to increase vascular permeability
C3b acts as an opsonin for phagocytosis
C5a recruits immune cells
C6-9 form the membrane attack complex
C1 complement binds a pathogen already opsonised with other serum proteins eg C-reactive protein (or Abs in adaptive)
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Complement components routinely deposited on cells are not degraded by the pathogen, allowing it to be recognised
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