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This patient's pruritic skin rash following wilderness exposure is consistent with poison ivy dermatitis, a form of contact dermatitis.  Poison ivy, poison oak, and poison sumac all produce urushiol, a small allergenic substance that causes an immune response when attached to proteins (ie, a hapten).  Following contact with these plants, patients develop a highly pruritic, erythematous rash consisting of papules, vesicles, and bullae that may show signs of excoriation.  The rash most frequently affects exposed skin (eg, legs, forearms) and often forms linear streaks as the patient walks past the plant, dragging it along the skin.

Contact dermatitis is a type IV (delayed-type) hypersensitivity reaction that occurs in 2 distinct phases:

1. The sensitization phase leads to the creation of hapten-specific T cells and takes 10-14 days.  Cutaneous dendritic cells take up the haptens and express them on MHC-I and MHC-II molecules as hapten-conjugated peptides.  These dendritic cells travel to the draining lymph nodes and interact with hapten-sensitive CD4+ and CD8+ T cells, causing activation and clonal expansion.
2. The elicitation phase occurs within 2-3 days following re-exposure to the same antigen (or following sensitization after first exposure to a highly antigenic antigen such as urushiol).  In this phase, the hapten is taken up by skin cells and causes activation of hapten-sensitized T cells in the dermis and epidermis.  This results in an inflammatory response and the clinical manifestations of contact dermatitis.

Depending on the etiologic agent, contact dermatitis can be mediated primarily by cytotoxic CD8+ T cells or CD4+ T_H1 cells (that cause indirect damage by activating macrophages).  In urushiol-induced contact dermatitis, CD8+ T cells are the primary effector cells and directly destroy keratinocytes expressing haptenated proteins.

(Choices A and C)  Mast cells and basophils, along with IgE, are primarily responsible for type I hypersensitivity allergic reactions.  Mast cells play a role in modulating the response in contact dermatitis by affecting antigen presentation and T-cell recruitment and activation, but they are not the main effector cells in type IV hypersensitivity.

(Choice B)  Eosinophils are cells that play a role in the defense against parasitic organisms and allergic reactions.

(Choice D)  Neutrophils are the primary phagocytic killers of the innate immune system and do not play a significant role in type IV hypersensitivity reactions.  They are more important in type III hypersensitivity reactions, in which deposited immune complexes activate complement and cause neutrophil-mediated tissue damage.

(Choice E)  Plasma cells are the principal cells responsible for the synthesis of immunoglobulins, which are directly responsible for type II and III hypersensitivity reactions.

Educational objective:
Poison ivy dermatitis is a form of allergic contact dermatitis, which is a type IV hypersensitivity reaction mediated primarily by T lymphocytes.  It manifests as intensely pruritic erythematous papules, vesicles, or bullae that often form linear patterns.