In Eczemasinduced by chemicals called haptens, endowed with reactive functions to self-proteins. Atopic eczema is induced by environment with proteins in contact of the. Industrialized countries have diseases are very common inflammatory dermatoses delayed hypersensitivity reactions leads this. The majority of individuals do not develop adaptive immunity and T lymphocytes (TL) following repeated contacts with specific allergens for tolerance, these inflammatory dermatoses are been induced in sensitized patients after recruitment and activation in the skin of cytotoxic LT (CTLs) that can induce apoptosis of keratinocytes with the allergen which immunohistological major characteristic of eczema.
Drug allergyare particularly interested in maculopapular exanthema (MPE), frequent and benign drug eruptions and DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms) or toxic epidermal necrolysis (TEN), rare but severe and engaging the prognosis in 30% of cases. The pathophysiological mechanisms that lead to the occurrence of these diseases after oral or parenteral administration of drugs remain few known, partly because of the lack of appropriate experimental models. The current paradigm posits that symptoms would develop according similar mechanisms to those described in eczema, with a central role of T cells specific to drugs in the development of skin lesions.
Methods followed foranimal testing in lab has a long expertise in the use and development of mouse models of allergic skin diseases, Translational medicine are used for patient samples such as blood, skin biopsies, blister liquid which are treat daily. Standard and new technologies are used to characterize skin and cell samples.
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