Random Dermatology MCQ - Type IV Hypersensitivity Reaction

A 48-hour-old, pruritic, erythematous, and vesicular rash develops at the site of a nickel-containing bracelet on a patient's wrist. A patch test to nickel is positive. Which of the following is the primary immunologic mechanism responsible for this reaction?

A) Type IV hypersensitivity reaction
B) Type I hypersensitivity reaction
C) Type II hypersensitivity reaction
D) Type III hypersensitivity reaction
E) Direct irritant effect

Correct Answer: A) Type IV hypersensitivity reaction

Explanation

This clinical scenario is a classic presentation of allergic contact dermatitis (ACD) to nickel, which is the prototype for a Type IV hypersensitivity reaction.

Key Features of Type IV Hypersensitivity (Delayed-Type):

• Mechanism: This is a T-cell-mediated reaction, specifically involving antigen-specific memory CD4+ T-helper 1 (Th1) cells and CD8+ cytotoxic T-cells.

• Time Course: The reaction is delayed, typically appearing 48-72 hours after antigen exposure. This delay is due to the time required for T-cells to be recruited to the site and release cytokines.

• Process:

  1. Sensitization Phase (First Exposure): The nickel hapten (incomplete antigen) penetrates the skin, binds to skin proteins, and is taken up by Langerhans cells (dendritic cells). These cells migrate to lymph nodes and present the antigen to naive T-cells, creating memory T-cells.

  2. Effector Phase (Subsequent Exposure): Upon re-exposure, the memory T-cells are activated, proliferate, and release cytokines (e.g., IFN-γ, TNF-α). This recruits other inflammatory cells (e.g., macrophages), leading to the characteristic spongiotic dermatitis (epidermal edema) and vesicle formation.

• Clinical Presentation: Pruritic, erythematous, papulovesicular rash confined to the area of contact.

Why Not the Other Options?

• (B) Type I hypersensitivity: An IgE-mediated immediate reaction (e.g., urticaria, allergic rhinitis). It occurs within minutes of exposure, not 48 hours.

• (C) Type II hypersensitivity: An antibody-mediated cytotoxic reaction (e.g., pemphigus vulgaris, bullous pemphigoid). Antibodies (IgG/IgM) bind to tissue antigens, leading to cell destruction.

• (D) Type III hypersensitivity: An immune complex-mediated reaction (e.g., serum sickness, vasculitis). Complexes of antigen and antibody (IgG/IgM) deposit in tissues, activating complement and attracting neutrophils.

• (E) Direct irritant effect: This is irritant contact dermatitis, which is non-immunologic. It can occur on first exposure in anyone if the irritant is strong enough and does not involve antigen-specific memory T-cells. A patch test would be negative.

Diagnosis and Management:

• Diagnosis: Confirmed by patch testing.

• Management: Avoidance of the allergen, topical corticosteroids for active flares.

Note: The delayed timing (48 hours) and the positive patch test are the key differentiators for a Type IV reaction. This mechanism is also responsible for the tuberculin skin test (PPD), graft-versus-host disease, and drug eruptions.