Background: Eczematous dermatitis including atopic dermatitis (AD) and allergic contact dermatitis (ACD) are characterized by T-cell infiltration into the dermis & epidermis. Although the effector pathways of activated T-cells have been intensively studied, the active role of epidermal keratinocytes (KC) in induction and maintenance of eczematous dermatitis has been rather neglected. It has been suggested that apoptosis of KC induced by T-cells and mediated by CD95 is crucial event in the transition from activation of the immune system to the manifestation of eczematous dermatitis. Objectives: The aim of this study is to assess the expression of Fas receptor (Fas-R) in the skin of eczematous dermatitis to help for the study of T-cell mediated KC apoptosis that might help for the future use of anti-apoptotic therapy for prevention and treatment of eczematous dermatitis. Methods: Thirty five patients with eczematous dermatits and fifteen age and sex matched controls were included. Full clinical examination was done and tissue levels of Fas-R and FasL were measured by quantitative real time -PCR. Results: In the current study, we observed that Fas-R and FasL were up-regulated in the cases group (p<0.001), (p<0.001) respectively compared to the controls. Fas-R and FasL were up -regulated in eczema cases (p=0.001), (p=0.001) respectively compared to the cases having other forms of eczematous dermatitis (CD and AD). On the other hand there was down regulation of Fas-R and FasL in CD cases (p=0.001), (p=0.001) respectively in comparison with the cases having other forms of eczematous dermatitis (eczema and AD). There was no significant relation between neither Fas-R nor FasL and any of the recorded variables, which include age, sex , or disease parameters including stage of disease, site, disease duration, redness, thickness, scratching and EASI score. Conclusions: Our study concludes that the up-regulation of Fas-R and FasL may be involved in the pathogenesis of eczema. This occurs through several mechanisms, including a possible unchecked pro-inflammatory TNF-α consequence. This means that Fas is responsible for initiation of eczematous dermatitis without being affected by age, sex and other variables of the disease as duration of disease and stage of the disease.