Atopic Dermatitis, Patch Testing, and House Dust Mites: A Brief Review

Alde Carlo P. Gavino; Glen R. Needham; Whitney A. High


Dermatitis. 2008;19(3):121-128. 

In This Article

AD and Immunity

AD is a chronic and recurrent skin disorder characterized histopathologically by an inflammatory T-cell infiltrate[6] which suggests a role for these cells in its pathogenesis. Patch testing has demonstrated that a specific sequential activation of T helper (Th) cells occurs in AD.[7,8] Within 24 hours of allergen exposure, interleukin-4 (a Th2 cytokine) messenger ribonucleic acid and protein levels in AD skin increase and then progressively decline to background levels over the next 24 hours. During this decline in Th2 cytokine production, the initially undetectable expression of interferon-γ (a Th1 cytokine) is markedly up-regulated. On the basis of this model, AD is believed to exhibit a biphasic immune pattern wherein a Th2 profile predominates at onset and during acute exacerbations whereas a Th1 profile prevails during chronic stages of the disease.[9,10]

Recently, the focus of research has shifted to the role of antigen-presenting cells (APCs), particularly dendritic cells (DCs) and skin-resident Langerhans' cells (LCs), in the pathogenesis of AD. LCs and DCs play a pivotal role in immunity by virtue of an ability to induce primary immune responses through the presentation of antigens to, and activation of, nave T cells.[11] Studies have demonstrated an up-regulation of the high-affinity immunoglobulin E receptor (FcɛRI) upon LCs and DCs present in lesional atopic skin but not among the same cells in nonlesional atopic skin or nonatopic skin.[12–14] This increased expression correlates with high serum immunoglobulin E (IgE) levels.[13] More importantly, it has been demonstrated that LCs and DCs present allergens to T cells 100- to 1,000-fold more effectively if the allergen is targeted to FcɛRI on these cells by allergen-specific IgE.[15] These phenotypic and functional characteristics equip LCs and DCs in AD with a markedly enhanced ability to initiate T-cell–mediated immune responses against allergens.


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