A 32-year-old woman comes to the allergy clinic due to a recurrent skin rash. The patient has had several episodes of itchy, erythematous, vesicular eruptions on her hands over the past several months. She works at a hair salon and is often exposed to hair dye and other beauty products. The patient has no other medical conditions and takes no medications. She undergoes patch testing, during which several allergens found in common cosmetic products are mounted on nonocclusive tape strips applied to her upper back. Skin findings developed after 2 days of application and are shown in the exhibit. Which of the following processes most likely occurred in this patient to enable the development of the observed skin reaction?
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This patient developed localized erythema and vesicles 2 days after reexposure to a chemical on patch testing, which identified the allergen responsible for allergic contact dermatitis (ACD). ACD is a type IV (delayed-type) hypersensitivity reaction that occurs in 2 phases:
In the sensitization phase, cutaneous Langerhans cells take up haptens (ie, allergens) and present them to naive CD4+ and CD8+ T cells in the regional lymph nodes, resulting in clonal expansion of hapten-sensitive T cells. This phase takes 10-14 days and does not result in cutaneous lesions.
On reexposure to the hapten, cutaneous antigen-presenting cells present the hapten to sensitized T cells recruited to the skin. When activated, these T cells mediate tissue damage that manifests as pruritic erythema, vesicles, and/or bullae. This elicitation phase occurs 2-3 days following reexposure to the hapten.
(Choices A and E) In type I (immediate) hypersensitivity reactions, initial allergen exposure leads to Th2 cell–induced, B-cell heavy-chain isotype switching and production of IgE, which subsequently binds to mast cells. This is accomplished in part by the binding of CD40 on B cells to CD40 ligand on T cells. On reexposure, allergens bind to IgE on mast cells and trigger immediate release of vasoactive peptides, resulting in urticaria (and anaphylaxis if severe). This inflammatory response is rapid (ie, minutes), unlike this patient's delayed (48-hr) response.
(Choice B) Bullous pemphigoid and pemphigus vulgaris are caused by autoantibodies against hemidesmosomes and desmosomes on keratinocytes, respectively. This causes epidermal/dermal separation and acantholysis, respectively, manifesting as bullae. These conditions are not type IV hypersensitive reactions and cannot be elicited by patch testing.
(Choice C) Immune complex deposition in small cutaneous vessels causes cutaneous small vessel vasculitis (CSVV). Medications that function as haptens (eg, phenytoin, sulfonamides) can cause the condition. Because of the extravasation of red blood cells due to vessel wall inflammation, CSVV presents with nonblanchable purpura and petechiae, not vesicles.
Educational objective:
Allergic contact dermatitis is a delayed-type hypersensitivity reaction. Initially, Langerhans cells travel to regional lymph nodes and present haptens to naive T cells, leading to clonal expansion. On reexposure to the hapten, sensitized T cells cause tissue destruction that manifests as pruritic erythema, vesicles, and/or bullae 2-3 days after exposure.