Read the summary and the most important questions on immunologie en celbiologie

• 1 Deeltoets 1

• 1.1 IMM 1

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• Innate: immediate vs induced

  Immediate: 
  -epithelial barriers
  - alternative pathway complement 
  -commensal micro-organisms
  -defensins
  
  induced:
  -scavenger receptors      
  -cytokines
  -lectin pathway complement
  -classical pathway complement

• Difference function B and T cells

  T cells form cellular defense
  B cells produce antibodies form the humoral defense

• Interactions between innate and adaptive immune system (2)

  1. Activation of adaptive immunity by innate dendritic cells
  2. Specific activation of innate immune cells by adaptive immunity: B- and T-cells

• Immune cells arise from two common progenitors during hematopoiesis (way of cell differentation)

  From the common myeloid cell precursor (innate) and the common lymphoid cell precursor (innate and adaptive)

• Common myeloid cell precursor: which immune cells arise? (5)

  Neutrophil, eosinophil, basophil, macrophage, dendritic cell (= innate)

• Common lymphoid cell precursor: which immune cells arise?

  B-cells, common (CD4) T-cell precursor, CD8 (=adaptive), NK-cells (=innate)

• C3 of complement: C3a

  C3 is the most important factor, it is cleaved into 3a and 3b.
  C3a = anaphylatoxin for immune cell recruitment. Enhances inflammation within minutes through activation of endothelium and immune cell recruitment. Increases blood vessel permeability (even as C5a),plasma proteins can go from blood into the infected site of the tissue C3a fragments are ligands for receptors on phagocytes, endothelial cells and mast cells. These bindings increase the inflammation.

• C3 of complement: C3b

  C3 is the most important factor, it is cleaved into 3a and 3b.
  C3b = pathogen binding for phagocytosis and lysis (destruction) of pathogen.
  Complement fixation leads to enhanced phagocytosis by binding complement receptors on the macrophages . CR binds C3b, these binding induces pathogen uptake, endo- or phagocytosis follows, degradation via fusion with acidic lysosomes.
  C3b is also important for formation of the membrane attack complex  (MAC) and pathogen lysis. When C3b binds C3 convertase, a new convertase is formed, which cleaves C5. C5 initiates formation MAC and lysis.

• Three pathways lead to complement activation

  1. Alternative pathway (spontaneous - hydrolysis)
  2. Lectin pathway (protein induced)
  3. Classical pathway (protein induced)

• Alternative pathway to complement activation

  Activated from onset of infection (so first to be activated). Environment at the pathogen surface alters C3 conformation to resemble that of activated C3b, through hydrolysis. Opsonized (= with a different surface) C3b is used to form membrane bound C3 convertase.
  So:
  C3 hydrolysis --> iC3,
  iC3 + inactive form of the complement protein factor B,
  factor B becomes susceptible to cleavage by protease factor D,
  a small fragment Ba (released) and a large fragment Bb are produced, Bb remains bound to iC3 --> iC3Bb,
  iC3Bb is a protease that specifically cleaves C3 into C3a and C3b fragments --> activation complement