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Pregled bibliografske jedinice broj: 147575

Overview on etiopathogenesis of atopic dermatitis

Lipozenčić Jasna; Paštar, Zrinjka; Ljubojević, Suzana; Batinac, Tanja
Overview on etiopathogenesis of atopic dermatitis // Acta Dermatovenerologica Croatica, 12 (2004), 118-119 (podatak o recenziji nije dostupan, kongresno priopcenje, stručni)

Overview on etiopathogenesis of atopic dermatitis

Lipozenčić Jasna ; Paštar, Zrinjka ; Ljubojević, Suzana ; Batinac, Tanja

Acta Dermatovenerologica Croatica (1330-027X) 12 (2004); 118-119

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, kongresno priopcenje, stručni

Ključne riječi
Etiopathogenesis of atopic dermatitis; genetic; environmental; skin barrier; pharmacologic; stress; emotional problems and immune factors

In the etiopathogenesis of atopic dermatitis (AD) there are well known interactions among genetic, environmental, skin barrier, pharmacologic, stress and other emotional problems and immune factors.Genetic determinate of expression of AD as a pure or mixed with concomitant respiratory or intestine allergy depends on genetic susceptibility. Although many genes are involved in the development of allergic diseases, there has been particular interest in chromosome 5q31-33, 3q21, 1q21 and 17q25.Immunologic abnormalities of type I and type IV reactions have been described in patients with AD. Immunologic triggers are aeroallergens, food allergens, microbial products, and autoallergens and contact allergens. The immunologic reactions determinate many features of AD, as well as a cell mediated or delayed hypersensitivity. Type 2 (TH2) and type 1 (TH1) cytokines contribute to the pathogenesis of skin inflammation in AD. The currently accepted model proposes a predominant TH2 cytokine milieu in the initiating stages or acute lesions of AD and a mixed TH1 and TH2 pattern in chronic lesions. This biphasic pattern of T cell activation has been demonstrated after epicutaneous application of aeroallergens using patch-test. After 24 hours increased expression of IL-4 mRNA and protein ; IL-5, IL-13 is observed, after which IL-4 expression declines to base levels. In contrast, IFN-γ mRNA is strongly expressed at the 48- to 72-h time points as development of TH1 lymphocytes is mediated by the cytokines IFN-γ and IL-2. Type 2 cytokines are thought to account for coincident eosinophilia and elevate IgE production and attraction of macrophages, which in turn produce IL-12, a known activator of the TH1-type immune response which suppress IgE production. So, AD skin contains an increased number of IgE-bearing Langerhans cells (LC) that, via the high-affinity IgE receptor FCє R1, is thought to bind allergens, as a major IgE binding receptor as there are several types of these receptors. LC play important role in cutaneous allergens presentation to TH2 cells via major histocompatibility molecules. These bridgings trigger a cascade of immunologic events. In chronic AD lesions LC are present in increased numbers and have increased amounts of IgE bound to high-affinity surface receptors. LC have been shown to be hyperstimulatory to helper T cells and can activate helper T cells to the TH2 phenotype in the initiating phase of the disease. Degranulation of eosinophils occurs in the dermis with the release of toxic proteins like major basic protein and could account for much of the inflammation. Mast cells are increased in number and produce mediators other than histamine that induce pruritus, and may have as effect on IFN-γ expression. Mast cells cytokines IL-4 and IL-13 are important for IgE production and mast cell chymase may induce eosinophil infiltration into AD lesional skin. There is elevated production of prostaglandin E2 (PGE2) by peripheral monocytes. Prostaglandin E2 (PGE2) has at least two potential roles in the initiation of AD. Firstly, it reduces IFN-γ production from helper T cells and thereby favoring initial, dominant TH2 immune response and, secondly, it directly enhances IgE production by B lymphocytes by increased secretion of IL-4, IL-5 and IL-13. Many lesions of AD result from scratching thereby it is tempting to speculate that immune perturbations in genetically predisposed individuals provoke the release of local pruritogens and keratinocyte-derived cytokines further drive the previously described immune response.

Izvorni jezik

Znanstvena područja
Kliničke medicinske znanosti


Projekt / tema

Medicinski fakultet, Zagreb

Časopis indeksira:

  • Scopus

Uključenost u ostale bibliografske baze podataka:

  • Excerpta Medica
  • Index Medicus