🫀Type II hypersensitivity

Question 1

What is the mechanism of type II hypersensitivity?

Answer 1

• Autoantibodies (IgG, IgM) → bind cell surface ags
• c’ activation → cell lysis / phagocytosis
• ADCC → NK cells/mps → cell destruction
• Ex: Hemolytic anemia, Graves’ disease, Myasthenia gravis

Question 2

How do IgG and IgM antibodies cause cell damage in type II reactions?

Answer 2

IgG/IgM bind Ag on host cell surface
→ c’ activation (C1q) → MAC → cell lysis
→ Opsonization → phagocytosis by macrophages
→ ADCC by NK cells → cell death

Question 3

What is antibody-dependent cellular cytotoxicity (ADCC)?

Answer 3

IgG binds target cell Ag
FcγR on NK cells binds IgG Fc
→ NK releases perforin, granzymes
→ Target cell apoptosis

Question 4

How does complement activation contribute to type II hypersensitivity?

Answer 4

IgG/IgM binds cell surface Ag → activates classical complement
→ C3b opsonisation → phagocytosis
→ C5b-9 (MAC) → cell lysis
→ C3a, C5a → inflammation (recruit neutrophils, ↑ vascular permeability)

Question 5

How does type II hypersensitivity contribute to rheumatic fever?

Answer 5

M protein (Strep pyogenes) mimics heart tissue (molecular mimicry)
→ IgG cross-reacts w/ cardiac Ag
→ inflammation → myocarditis, valvulitis
Type II HS: Ab-mediated tissue injury (no active infection present)

Question 6

Why is the Rh incompatibility reaction in pregnancy a type II hypersensitivity?

Answer 6

Fetal Rh⁺ RBCs enter maternal Rh⁻ circulation → IgG anti-Rh produced

In 2nd pregnancy, IgG crosses placenta → binds fetal RBCs
→ Complement activation, phagocytosis → hemolysis

Classic Type II HS: Ab (IgG) targets cell-bound Ag → cell destruction