Hypersensitivity Overview

Hypersensitivity Overview

• Hypersensitivity is an exaggerated or inappropriate immune response to antigens.
• Four types exist: Type I, Type II, Type III, and Type IV.

Type I Hypersensitivity

• Mechanism: IgE-mediated, fast onset (seconds to minutes).
• Mediators: Mast cells and basophils release histamine, leukotrienes, and prostaglandins.
• Examples: Anaphylaxis, asthma.

Type II Hypersensitivity

• Mechanism: IgG or IgM antibodies bind to cell surface antigens, activating complement or phagocytosis.
• Examples: Hemolytic anemia, Rh incompatibility.
• Mediators: IgG, IgM, complement

Type III Hypersensitivity

• Mechanism: Antigen-antibody complexes deposit in tissues, causing inflammation.
• Triggers: Foreign proteins or drugs.
• Examples: Serum sickness, Post-Streptococcal Glomerulonephritis (PSGN).
• Mediators: Antigen-antibody complexes, complement.

Type IV Hypersensitivity

• Mechanism: T-cell-mediated, delayed onset (48-72 hours).
• Examples: Contact dermatitis, tuberculin skin test.
• Mediators: T cells release cytokines, activating macrophages.

Clinical Manifestations

• Anaphylaxis (Type I): Symptoms include hypotension, airway constriction, and urticaria (hives). Mediators include histamine and leukotrienes. Treatment involves epinephrine, antihistamines, and corticosteroids.

• Hemolytic Anemia (Type II): Symptoms include fatigue, jaundice, pallor, and dark urine. Mediators involve IgG, IgM, and complement. Examples include Rh incompatibility and blood transfusion reactions

• Serum Sickness (Type III): Symptoms are fever, rash, joint pain, and swollen lymph nodes. A trigger is often foreign proteins/drugs.

• Contact Dermatitis (Type IV): Characterized by a red, itchy, and vesicular rash. Common triggers include allergens like poison ivy or nickel. Treatment usually involves avoiding the allergen & topical steroids.

Immune Mediators and Mechanisms

• Type I: IgE triggers mast cells/basophils releasing histamine, leukotrienes, and prostaglandins.
• Type II: IgG/IgM activates complement or phagocytosis
• Type III: Immune complexes activate complement and recruit neutrophils
• Type IV: T cells release cytokines, activating macrophages

Key Concepts for Differentiation

• Mediators: Antibodies (Types I-III), T cells (Type IV).
• Onset: Immediate (Type I) to delayed (Type IV).
• Treatment: Antihistamines (Type I), Steroids (all types), Immunosuppressants (Type IV), Biologics (target specific mediators).

Cytokines and Complements

• Cytokines:

  • IL-4 drives IgE production (Type I).
  • TNF-α enhances inflammation (Types II, III).
  • IFN-γ activates macrophages (Type IV).

• Complement System: Cascade of proteins that identifies and destroys pathogens; crucial in Types II and III.

Test Tips

1. Memorize the immune mediators for each type (e.g., IgE for Type I, IgG/IgM for Types II & III, T cells for Type IV).
2. Understand the examples and symptoms of each hypersensitivity type.
3. Be familiar with the time of onset and specific triggers for each hypersensitivity type.
4. Know the therapeutic interventions and their rationale.

This quiz explores the four types of hypersensitivity and their mechanisms. It covers Type I, II, III, and IV responses in detail, highlighting examples and mediators for each type. Test your understanding of immune responses and their implications.