Lecture 22 - Hypersensitivity Type Ii

HYPERSENSITIVITY TYPE II

Difference between types I-III, Ig isotype involved.

hypersensitivity

Clinical

reaction

Mediator

manifestation

I

IgE

Urticaria,

II

IgM, IgG

hemolytic anemia

III

IgM, IgG

serum sickness

IV

TDTH

contact dermatitis

Difference between types II & III, Type II- Ab directed to cell surface antigens on specific tissues (Antibody-mediated hypersensitivity) Type III- Ab bind to soluble antigens forming immune complexes, deposited in various tissues (Immune-complex mediated hypersensitivity)

Hypersensitivity Type II I

Complement activation MAC formation

II Complement activation Opsonisation Anaphylatoxin release ADCC III

ADCC

Clinical manifestations: 1. Transfusion Reactions Caused by glyco-proteins found on RBCs in different allelic forms (ABO system)

ABO blood groups Genotype Blood group Ag on RBCs Serum Ab phenotype AA or AO

A

A

Anti-B

BB or BO

B

B

Anti-A

AB OO

AB O

A&B None

None Anti-A & Anti-B

anti-RBCs cause hemolysis Clinical manifestations: associated with ABO incompatibility resulting in intravascular

hemolysis,

Hb

in

plasma,

hemoglobinuria

Transfusion reactions can be prevented by proper cross-matching

2.

Drug-induced

hemolytic

Caused by some antibiotics (e.g. penicillin, cephalosporin, streptomycin), adsorb nonspecifically to proteins on RBCs, lead to Cmediated lysis & severe anemia

anemia

3. Auto-immune diseases Examples: Grave’s Disease

Auto-Ab to TSH

Goodpasture’s syndrome Auto-Ab to Glomerular Basement Membrane in kidney & lung Myasthenia Gravis

Auto-Ab to acetylcholine receptor