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Immunological Events

Amber Jade Lewis Flashcards 6 Englisch 74 Karten

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  1. 1How does immediate innate immunity act?Takes 0-4 hours
    Infection causes recognition by non-specific effectors leading to removal of infectious agents
  2. 2How does early induced innate immunity act?Infection leads to PAMP recognition leading to inflammatory recruitment and removal of infectious agent
  3. 3How does adaptive immunity act?Infection leads to detective in the lymphoid organs and Ag recognition by Niave B and T-cells, clonal expansion, removal of infection & induced memory
  4. 4How are soluble and cellular elements of the innate immune system activated?Triggered by infectious agents bearing pathogen associated molecular patterns (PAMPs) eg: bacterial and fungal cell wall components such as lipopolysaccharide, mannose, flagellae and genetic material
  5. 5What host molecules recognise these components?Pattern recognition molecules
    Serum protein c-reactive protein (crp)
    Complement components, mannose binding lectin and cellular receptors, PRRs on macrophages, neutrophils, NK cells, dentritic cells, etc
  6. 6What do TLRs induce?NFkB
  7. 7What is the role of TLR's?They bind to pathogen components (11 of which are PRR's)
  8. 8What are the key cells expressing TLR's?Macrophages, neutrophils, dendritic cells, mast cells and b-cells
  9. 9What do TLR's trigger?TLR's trigger production of inflammatory cytokines IL-1, TNF, chemokines, interferon and adhesion molecules
    They also enhance Ag presintation by APC's and co-stimulation molecules
  10. 10How does LPS stimulate immune response?Stimulates TLR-4 by LBS-binding protein, the LPS;LBS complex interacts with TLR-4 resulting in a immune response
  11. 11What are NOD receptors?Bacterial peptidoglycan recognisers
    Induce NFkB
  12. 12What do RIG-1 and MDA-5 do?Induce NFkB
    Cytoplasmic receptors detect viral DNA
    Viral DNA binds RIG-1 induces assoication with adaptor MAVs causing dimerization, MAVs induces inflammatory cytokines and interferons
  13. 13What do interferon a-leuokocytes and B-fibroblasts do?Produced by virally infected cells and activate antiviral mechanisms in surrounding cells preventing spreading
    They produce PKR causing apoptosis or blocking viral protein synthesis, oligoadenylates RNASE which degrades viral mRNA and MX protein blocking viral transcription
  14. 14What is complement involved in?Killing bacteria and viruses via formation of membrane attack complex
    Opsoninsation with C3a and C4b
    Inflammation with anaphylatoxins C3a, C4a and C5a
  15. 15What is the classical pathway?Antigen-antibody complex
  16. 16What is the lectin pathway?Mannose-binding lectin binds carbohydrates on pathogen surfaces
  17. 17What is the alternative pathway?Pathogen surfaces
  18. 18What do the classical, lectin and alternative pathway all lead to?C3 convertase and then peptide mediators of inflammatory processes (C3/5a)
    Opsoninsation and removal of immune complexes (C3b)
    Membrane attack complex
  19. 19What molecules undergo phagocytosis?Macrophages and neutrophils
  20. 20How is phagocytosis carried out?PAMPs on pathogens are recognised, they are bound, engulfed and destroyed
  21. 21What do PAMPs also lead to?Cellular activation
  22. 22What mechanisms exist for macrophage killing?Oxygen dependent and oxygen independent
    Activation leads to release of cytokines
  23. 23What does IL-1B do?Activates vascular endothelium lymphs
  24. 24What does TNF-a do?Activates vascular endothelium and permeability leading to entry of IgG, complement to tissues and increased fluid drainage
  25. 25What does IL-6 do?Lymph activation and antibody production
  26. 26What does CXCL8 do?Recruits neutrophils, basophils and t-cells
  27. 27What does IL-12 do?Activates NK cells and differentation of CD4 cells to Th1 cells
  28. 28What are acute phase proteins?Produced in the liver and generally increase on infection and stress, often in response to cytokines (IL-6) from macrophages
    Help in defense against microorganisms limiting tissue damage
  29. 29What does C-reactive protein do?Activates complement opsoninsation
  30. 30What is Mannose binding protein?Activates complement/ opsonin
  31. 31What are metal binding proteins?Caeruloplasmin
  32. 32What are protease inhibitors?Protease inhibitors
  33. 33What are natural killer cells?Large granular lymphocytes
    Kill virally infected cells without Ag activation, they recognise reduced MHC class I on virally infected cells
    Active without activation however can be activated by ctokines (IL-2/12/15, IFN)
  34. 34What are the killing mechanisms of NK cells?Perforin-mediated killing to target cell apoptosis
    Fas-receptor mediated killing
    TNF-mediated killing
    Antibody-dependent cell-mediated cytotoxicity (ADCC)
    Also secrete IFNy limiting viral spread
  35. 35What is inflammation the consequence of?Induced innate response
  36. 36What is inflammation induced as part of the immune response?General defence mechanism against infection and injury, involves marshalling of leukocytes, plasma and plasma proteins fight against infection and repair damage
  37. 37What is inflammation mediated by?Stimulation of TLRs leading to production of cytokines, cytokines and other mediators
    Activation of inflammasome to activate proforms of inflammatory cytokines IL-8/1
    Activation of complement producing inflammatory mediators activating mast cells
  38. 38What is bacterial septic shock?Produced as a result of bacterial cell wall endotoxins (LPS) stimulating production of cytokines (IL-1 and TNF) from macrophages in the liver and the spleen
  39. 39When does this usually occur?Occurs within a few hours of infection where it has spread to bloodstream
  40. 40What causes septic shock?Gram -ve bacteria such as E.coli, Klebsiella pneumoniae, pseudomonas aeruginosa and Neisseria meningitidis
  41. 41What are the symptoms?Drop in blood pressure, fever and widespread clotting, haemmorrhagic necrosis, multiple organ failure
  42. 42What is the role of TNF in septic shock in a local infection?Macrophages activated and secrete TNFa into the tissue releasing plasma proteins, increased platelet adhesion, phagocytosis of bacteria and local vessel occlusion. Plasma and cells drain to lymph nodes and infection is removed
  43. 43What is the role of TNF-a in systemic infections?Macrophages in liver and spleen secrete TNF-a into the bloodstream, systemic oedema causes decreased blood volume, hypoproteinemia, netropenia and collapse of vessels. Disseminated intravascular coagulation occurs leading to multiple organ failure
  44. 44What are cytokine storms?Happen in bacterial/ viral infections
    Release highly elevated levels of cytokines eg: IL-1B, TNFa, IL-6 and CCL8
    Involved in septic shock, toxic shock and respiratory distress
  45. 45What are the symptoms of this?Fever, rash, drop in blood pressure, blood clotting and organ failure
  46. 46What is the role of dendritic cells?Antigen presenting cells
    Provide link between innate & adaptive
    Process & present Ag for t-cell activation
    Immature cells take up external microoganisms by phagocytosis and macropinocytosis
  47. 47How does activation and maturation occur?Via PAMPS, TLR signalling and IL-1/TNF stimulation
  48. 48What happens on activation and maturation?Dendritic cells lose phagocytic receptors migrate to lymph nodes, gain co-stim receptors, changing from antigen processing cells to mature APC's
  49. 49What do bacterial, viral and fungi antigens release?Bacterial and viral Ag release IL-12 bind naive t-cells, activating Th1, IFNy
    Fungi Ags release IL-6/23 bind naive t-cells activating Th17and IL-17 or induce IL-10, RA,TGF-B
  50. 50What is the role of TH1IFN-Y and macrophage stimulation = kill bacteria
  51. 51What is the role of TH2?IL-4/5/13 stimulating eosinophils, mast cells and plasma cells
  52. 52What is the role of TH17?IL-17 & fibroblasts = chemokine and neutrophil activation
  53. 53What is the role of TfH?Binds b-cells causing class switching and affinity maturation
  54. 54What is the role of T-regs?Inhibit immature dendritic cells (lack of activation)
  55. 55What happens in the sensitization stage?T-helper mediates
  56. 56What happens in the efforter stage?Sensitized t-helper cells secrete chemokines and cytokines
  57. 57What does IFN-y and CD40 ligand do?Activates macrophages to destroy engulfed bacteria
  58. 58What does the FAS ligand of LT-a do?Kills chronically infected cells releasing bacteria to be destory by fresh macrophages
  59. 59What does IL-2 do?Induces T-cell proliferation, increading number of effector cells
  60. 60What does IL-3 and GM-CSF do?Induces macrophage differenation in the marrow
  61. 61What do cytotoxic t-cells do?Tc cells kill virally and bacterially infected cells
    Produced 3-4 days after infection
    They recongnise proteins processed and presented in association with MHC class I molecules (specific)
  62. 62What are the killing mechanisms?Similar to NK cells
    They may also produce granulysin in the granules which can kill bacteria
  63. 63What are antibodies?Secreted by plasma cells produced by activated B-cells
    They provide protection from extracellular microorganisms
  64. 64How to B-cells produce antibodies?B-cells recognise specific micro-organisms via specific B-cells receptors or membrane immunoglobulins or surface immunoglobins
    On activation they diffentriate into plasma cells which secrete antibody of the same specificity as the surface antibody & memory
    B-cell activation, proliferation and maturation into plasma cells and memory cells occur in secondary lymphoid tissues and organs
  65. 65How are B-cells activated?Antigen recognition induces expression of effector molecules by the T-helper cells which activates the B-cell
  66. 66What activates B-cells?Thymus dependent Ags
  67. 67What are type I thymus independent Ags?They bind to B-cells via Ig and initate receptors such as TLRs to produce activation
  68. 68What are type II thymus independent AgsLinear Ags not easily degraded with spaces repeating antigenic determinants
  69. 69How do thymus dependent Ags work?They activate B-cells independent of B-cell specificity and T-helper cells providing rapid protection (IgM antibodies)
  70. 70How do B-cells remove micro-organisms?Neutralisation
    Opsonization
    Complement
    May also prevent binding to host and prevent the bacteria obtaining nutrients
  71. 71What is neutralisation?Toxins
    Ingestion by macrophages
  72. 72What is opsonization?Ingestion by macrophages
    Bacteria
  73. 73What is complement?Bacteria in plasma
    Lysis and ingestion
  74. 74What is antibody dependent cell mediated cytotoxicity ADCC?Occurs when cells with Fc receptors bind to an antibody on an antibody coated targeted cell
    Cells involved include NK cells, macrophage, neutrophils and eosinophils
    Antibody may be viral and bacterial Ag or infection cell components of worms

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6 Flashcards Karteikarten am Immunological Events, erstellt von Amber Jade Lewis am 02/01/2016.
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