AD is a chronic inflammatory disease associated with dry and itchy skin. An altered lipid composition is responsible of the xerotic aspect of the skin in atopic patients, and determines an increased permeability to topical allergens or irritants, thus inevitably leading to the production of many proinflammatory mediators by resident cells. Moreover, a deranged synthesis of cell membrane lipids can help to explain the propensity of AD keratinocytes to an exaggerated release of cytokines and chemokines, a phenomenon that in vivo can have a major role in promoting inflammatory processes. Specific immune responses against a variety of environmental allergens are implicated in AD pathogenesis in a relevant percentage of patients. A dysregulation in cytokine production has been widely documented in peripheral blood mononuclear cells of these patients, and a number of reports have focused on unbalanced populations of allergen-specific Th1 and Th2 subsets in favour of Th2. Notably, activated DC are a major component of lesional skin infiltrate. Thanks to their surface expression of specific IgE receptors, these cells play a critical role in the amplification of antigen-specific T cell activation. Cross-linkage of specific IgE receptors on dermal mast cells during hypersensitivity reaction provoke their degranulation, with a subsequent release of a vast series of mediators and cytokines. Following a process of recruitment and activation into the inflammatory site, eosinophils are also thought to contribute relevantly to skin damage. A complex system of cytokines and chemokines contributes to establish a local milieu that favours the permanence of skin inflammation. Genetic studies have recently demonstrated that a particularly complex background underlies the atopic syndrome through an altered control on IgE-mediated responses. So far, the genetic basis to explain the intrinsically altered response of AD keratinocytes to inflammation is unknown.
|Number of pages||7|
|Journal||EOS Rivista di Immunologia ed Immunofarmacologia|
|Publication status||Published - 1999|
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