Abstract

Despite the requirement for prior contact with an allergen for sensitization to occur, the majority of peanut allergic children react to their first known peanut ingestion. Evidence suggests that sensitization may occur by contact with allergen through the skin. Individuals thus sensitized may be predisposed to developing peanut allergy, whilst tolerance to peanut may be induced by oral exposure. We employ the use of skin and gastrointestinal homing memory T cell markers (Cutaneous Lymphocyte Antigen (CLA) and α4β7 respectively) to indicate the likely route of initial sensitization and examine the evidence for this theory. Immunomagnetic beads are used to isolate CLA+ and α4β7+ memory T cells from peripheral blood mononuclear cells. The cells are stimulated with peanut extract in the presence of antigen presenting cells. Thymidine incorporation is assayed to measure lymphocyte proliferation. Stimulation indices to peanut in the CLA+ cells are compared to those in the α4β7+ cells in both peanut allergic and peanut tolerant children. Peanut specific cytokine production including IL4, IL5, IFN-γ, TFN-α, IL10 and TGF-β is batched and measured in the cell culture supernatants of both groups. Higher proliferation is observed in the CLA+ memory T cells relative to the α4β7+ memory T cells in peanut allergy. This trend appears to be reversed in non-allergic patients. In vitro evidence supports the hypothesis that sensitization to peanut via the skin may be associated with the development of peanut allergy, whilst oral sensitization may induce tolerance. Such studies may help to facilitate the diagnosis of peanut allergy.

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