🫀Type III hypersensitivity

Question 1

What is the mechanism of type III hypersensitivity?

Answer 1

• Ag-Ab (IgG/IgM) complexes form in circulation
• Deposit in tissues (e.g. kidney, joints, vessels)
→ c’ activation → C3a, C5a recruit neutrophils
→ inflamm & tissue dmg (e.g. vasculitis, GN)

Question 2

How do immune complexes cause tissue damage?

Answer 2

ICs deposit in tissues → activate c’
• C3a, C5a recruit neutrophils → release ROS, enzymes
→ Inflammation & tissue dmg (e.g. vasculitis, nephritis)’

Question 3

What is the role of complement in type III reactions?

Answer 3

ICs → activate complement (esp. C3, C5)
• C3a, C5a = anaphylatoxins → recruit Ns + ↑ vascular permeability
→ inflamm & tissue injury

Question 4

What is the Arthus reaction?

Answer 4

Local type III HS reaction (in skin)
• Ag + pre-formed IgG → immune complexes → c’ activation
→ inflamm, edema, necrosis at injection site

Question 5

How does SLE involve type III hypersensitivity mechanisms?

Answer 5

Autoantibodies (e.g. anti-dsDNA) bind self Ags → ICs
→ deposit in tissues (e.g. kidney, skin, joints)
→ c’ activation (C3a, C5a) → inflammation, tissue damage

Question 6

What are clinical consequences of immune complex deposition?

Answer 6

• inflamm: Tissue damage (e.g. vasculitis, glomerulonephritis)
• Organ dysfn: Kidney failure, skin rashes (e.g. butterfly rash in SLE)
• Pain/swelling: Joint inflammation (e.g. arthritis-like symptoms)
• Chronic dmg: Progressive organ failure (e.g. renal, vascular)