Chapter 16

Question 1

How are autoimmune diseases grouped?

Answer 1

• categories II-IV
  
  • like hypersensitivities
  • no autoimmune disease is mediated by IgE (no cat. I)

Question 2

Lack of which transcription factor can cause autoimmune diseases?

Answer 2

• AIRE = responsible for removal of thymocytes that bind self-antigens
  
  • induces deletion
  • makes sure self proteins for negative selection are expressed in thymus
• loss of T cell self tolerance

Question 3

Which T cells initiate autoimmune response?

Answer 3

• TH17 CD4 T cells
  
  • most inflammatory
  • regulated by Treg (both dependent on TGF-B)
    
    • FoxP3 unique for Treg
• mutation of FoxP3 gene -> autoimmune diseases (lack of control)

Question 4

Which gene mutation increases susceptibility to autoimmune diseases?

Answer 4

• HLA
  
  • present antigens to T cells
  • potentially modify the peptide before presenting it -> recognised as non self

Question 5

Which immune cell tolerance is most important in preventing autoimmunity?

Answer 5

• T cell tolerance
  
  • efficient process of elimination of T cells binding to self antigens -> prevents activation of B cells
  • association with HLA
    
    • more autoimmune diseases associated with HLA class II (CD4 T cells) -> lower threshold to activate CD4 T cells
  • some T cells may have a higher sensitivity (need more antigen)
    
    • inflammation -> MHC class II expressed on more cells (activation of self T cells with high sensitivity)

Question 6

What happens when autoantibodies bind to receptors on cells?

Answer 6

• receptor agonist: mimic ligand -> activating signal
• receptor antagonists: block ligand binding -> no activation

Question 7

What is epitope spreading?

Answer 7

• in autoimmune disease
• antibodies bind one part of an antigenic molecule
  
  • then progresses to different epitopes -> causing disease

Question 8

What is intermolecular epitope spreading?

Answer 8

• initially self antigens on cell surface are bound -> inflammatory reaction -> cell death
• cellular antigens released -> form immune complexes with self reactive antibodies
  
  • deposition in blood vessels, kidneys, joints -> more inflammation
  • cell releases man macromolecules (potential autoantigens) -> antibody made against one of them binds
    
    • delivers particle to cells -> facilitates development of antibodies against other components
    • when T cell binds to B cell presenting antigen it can help B cell take up other components -> make new antigens