Applied parasitology - immune mediated diseases

6 important questions on Applied parasitology - immune mediated diseases

Properties of Atopic diseases:

  • Fast hypersensitive response because of genetic tendency to produce IgE
  • specific to 'harmless' antigens abundantly present in environment
  • often type 2 immunity (asthma, hay fever, food allergies)

What happens with Atopic diseases for first and second time exposure?

  • First time exposure -> allergen binds to Th2 -> B cell activated -> IgE produced -> Mast cells/basophils (FcR) are activated = sensitization
  • Second time exposure: mast cell/basophil (FcR) sensitized -> degranulation of prostaglandins, histamines, cytokines and chemokines -> acute inflammatory response -> hypersensitivity

What are autoimmune diseases and how are they developed?

There is a loss op discrimination between self and non-self cells -> type 1 immunity (e.g. Diabetes type 1 and multiple sclerosis)

Development: unbalanced immune response by reduced susceptibility of Treg (regulatory T cells) by T-effector cells.
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What happens with type 2 immune response against helminths?

Polarisation of Th2, alternative activation of macrophages, IgE antibodies are produced -> activation of mast cells and eosinophils (kill the worm) via surface bound IgE

What happens in the first line of defence immune modulation?

Damage to the epithelium triggers the release of alarmins -> alarmins stimulate type 2 immunity -> type 2 cytokines in turn activate goblet cells to produce mucus -> activation of smooth muscle cells -> weep and sweep response (helminths are expelled alive)

Helminths have components in their saliva that stop the release of alarmins -> stops type 2 immune response

What happens in the second line of defence immune modulation?

Dendritic cells induce type 2 immunity ->
alternatively activated macrophages for enhanced wound healing (also produce anti-inflammatory cytokines) -> eosinophils kill helminths

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