Autoimmunity

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  • Created by: Emma Gill
  • Created on: 12-05-13 16:27

Autoimmunity

This is due to either a deficit in central or peripheral tolerance and the cause is usually genetic. It is characterized as type II hypersensitivity reaction and normally presents at a young age.  

Central Tolerance

  • Thymocytes and medullary epithelial cells in thymus cannot present TRAs so no negative selection
  • Lack of AIRE gene leads to APECED
  • Symptoms: allopecia, diabetes, graves disease, addisons disease
  • 

Peripheral Tolerance

  • Lack of regulatory T-cells: cannot induce apoptosis in self-T-cellactivated  in without costimulation
  • Lack of foxp3 gene leads to IPEX
  • Symptoms: allopecia, diabetes, graves disease, addisons disease, IBS
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Autoimmunity

This is due to either a deficit in central or peripheral tolerance and the cause is usually genetic. It is characterized as type II hypersensitivity reaction and normally presents at a young age.  

Central Tolerance

  • Thymocytes and medullary epithelial cells in thymus cannot present TRAs so no negative selection
  • Lack of AIRE gene leads to APECED
  • Symptoms: allopecia, diabetes, graves disease, addisons disease
  • 

Peripheral Tolerance

  • Lack of regulatory T-cells: cannot induce apoptosis in self-T-cellactivated  in without costimulation
  • Lack of foxp3 gene leads to IPEX, X-linked so only affects males
  • Symptoms: allopecia, diabetes, graves disease, addisons disease, IBS
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Primary Immunodeficiency

Genetic defect in component of immune system, X-linked in 70% of cases, presents in the young.

Cellular

  • Chronic granulomatous disease (neutrophils lack cytochrome b and hydrogen peroxide)
  • SCID (adenose deaminase deficiency essential for lymphocyte production)
  • X-SCID (IL-2RG encodes y-chain for cytokine receptors so T-cells not activated)
  • Leukocyte adhesion defect (lack of adhesion molecules so struggle to enter tissue)

Lymphoid

  • Di Georges Syndrome (no thymus due to lack of CATCH22 gene therefore no mature T-cells)

Soluble Mediator

  • Bare lymphocyte Syndrome: No MHCII, Agammaglobulinaemia (no Ig), IgA deficiency
  • Complement deficiency or Cytokine deficiency
  • TLR, MBL defects alter innate immunity along with CAM defects
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