الفهرس 
The three phases of atopic dermatitisOnly 14 pages are availabe for public view
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Abstract
A
topic dermatitis (AD) is a chronic relapsing, pruritic, inflammatory skin disease. It is associated with personal or family history of other atopic diseases.It results from a complex interplay between genetic and environmental factors.
IL-4, IL-5 and IL-13 cytokines play a role in the TH2 response which is seen in the early stages of AD. Chronic AD lesions principally have a TH1 response with the cytokines IL-12 and interferon-g playing a dominant role.
Complex interactions among genetic, environ-mental, altered skin barrier and immunologic factors, stress and other emotional problems contribute to the pathogenosis of AD.The diagnosis of atopic dermatitis (AD) is rarely aided by investigations.
Defensins are broadly dispersed family of antimicrobial peptides. Defensins are classified into 3 distinct families: the α-defensins, the β-defensins, and the theta defensins. The first isolated human β-defensin is, HBD-1 was purified from human plasma in 1995. Its expression was subsequently detected in epithelial cells derived from the kidney, female reproductive tract, respiratory tract, pancreas and in other tissues. Defensins differ in their discovery, classification, molecular properties, expression, mechanisms of action and potential medical applications.
Defensins were proved to be -Key Components of innate and adaptive Immunity by promoting chemokine production and chemotaxis and by Interacting with effector cells of the innate immune response.
The primary function of defensins is to protect the skin from invasion by foreign pathogens. In addition to their microbicidal function, defensins also modulate immune functions.
Polymorphisms in HBD1 gene (SNPs) were proved to be associated with atopic dermatitis.Two interesting SNPs which are DEFB1 692 A à G and DEFB1 1654 G à A.
Our study was preformed on 35 atopic patients and 13 10 healthy volunteers as controls. We observed that G allele at site 692 is associated with AD susceptibility and that AA genotype at both sites (692, 1654 of DEFB1 has low frequency in AD. significant difference in the distribution of the DEFB1 A/G polymorphism at site 692 in AD patients when was compared with controls. In contrast, we observed no significant difference in the distribution of the DEFB1 A/G polymorphism at site 1654 on AD patients when was compared with control.
In the present study, we found that AA genotype is associated with low severity index. However, AA genotype at site 1654 is associatd with high severity index.
We recommend to repeat the present study in a larger sample size and to access genetic components in combination with environmental factors that trigger AD. the association of DEFB1 A/G polymorphism at site 692 with AD severity proved to be non significant. In contrast, we observed significant association between DEFB1 A/G polymorphism at site 1654 with AD severity.
As regard DEFB1 A/G polymorphism at site 692 we found that GG genotype is associated with AD susceptibility and atopy. Also we found that the AA genotype at site 1654 is associated with atopy and disease severity. It seems that DEFB1 has an important role in skin inflammation and the responsiveness to the allergens.
In the present study, we didn’t find any correlation between serum total IgE level and DEFB1 gene polymorphism at both sites (692 and 1654). However, we found significant statistical association between DEFB1 genotypes at site 692 and 1654 and specificIgE.