Hypersensitivity 3 and 4

Question 1

Type III hypersensitivity:

Answer 1

Immune Complex Mediated Hypersensitivity

• Involves IgG or IgM antibodies that react with soluble antigens to form immune complexes that are deposited in tissues.
• Complement and Fc-mediated inflammation leads to tissue damage.
• Can be systemic or localized.

Question 2

Deposition of immune complexes - favored sites (5):

Answer 2

1. Kidneys.
2. Joints.
3. Small vessels.
4. Heart.
5. Skin.

Question 3

Type III hypersensitivity disease associations (6):

Answer 3

1. Serum sickness.
2. Drug reactions.
3. Rheumatic arthritis.
4. Systemic lupus erythematosus.
5. Post-streptococcal GN
6. Polyarteritis nodosum.

Question 4

Serum sickness:

Answer 4

• Antigen-antibody complexes form in circulation and deposit in tissues.
• Complement levels in serum decrease due to activation.
• Eventually excess antibody limits formation of complexes.

Question 5

Serum sickness clinical manifestations:

Answer 5

• Rash.
• Fever.
• Arthralgia or arthritis.
• 1-2 weeks after first exposure.

Question 6

Drug reactions:

Answer 6

• A type of serum sickness caused by hypersensitivity to an IV injection of a drug.
• Particularly antibiotics.
• Caused by drug-specific immune complexes.
• Small drug molecules may serve as haptens that bind to serum proteins that then develop antibody response either to the hapten or the hapten-protein conjugate.

Question 7

Rheumatoid arthritis:

Answer 7

Autoimmune disease characterized by chronically inflamed synovium.
- IgM which has specificity for determinants on the Fc portion of the pt’s own IgG is called rheumatic factor and is deposited in joints.

Question 8

Systemic lupus erythematosus:

Answer 8

• Chronic inflammatory disease targeting mainly joints, kidneys, heart, skin and lung.
• Autoantibodies to multiple nuclear antigens, including double-stranded DNA.
• Antigen/antibody complexes damage tissues by activating complement and by engaging Fc receptors on immune cells expressing these receptors.

Question 9

Post-streptococcal glomerulonephritis:

Answer 9

PSGN

• Associated with group A strep.
• Immune complexes deposit in the lipid bilayer of the glomerular basement membrane.
• Activation of the classical complement pathway leads to damage to the basement membrane.
• Abrupt onset of symptoms 1-4 weeks after infection.
• Dark or smokey colored urine.

Question 10

Type IV hypersensitivity:

Answer 10

Delayed Type Hypersensitivity or T Cell-Mediated

• Initiated by antigen specific Th1 cells.
• T cells and macrophages are the major cellular mediators.
• Cytokines amplify and continue response.

Question 11

Hallmarks of Type IV hypersensitivity (4):

Answer 11

1. Delay in time required for the reaction to develop to re-exposure to antigen.
2. The recruitment of macrophages as opposed to neutrophils.
3. Extensive tissue damage.
4. Associated with cytokines.

Question 12

Diseases associated with Type IV hypersensitivity (6):

Answer 12

1. Contact dermatitis.
2. MS.
3. Type I diabetes.
4. Rheumatoid arthritis.
5. Graph rejection.
6. Tumor immunity.