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Received Oct 1, 2017; Accepted Jan 3, 2018
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1. Introduction
Atopic dermatitis (AD) is the most common chronic allergic and inflammatory disease of the skin and often further precedes allergic diseases [1, 2]. Atopic dermatitis is characterized by epidermal barrier dysfunction, cutaneous inflammation, and pruritus (itch and rashes), which is a hallmark of AD. These symptoms lead to excoriations, inflammation, and disease worsening [3–5]. AD has been proven to be strongly associated with increased prevalence of comorbidities, including immunoglobulin E- (IgE-) related diseases (atopy), skin inflammation and infections, and mental disorders [6, 7]. The prevalence of AD is high in many countries, based on several studies with data from over one million children from 97 countries [8, 9]. The global prevalence of AD is approximately 15–30% in children and approximately 10% in adults [10, 11]. The pathogenesis of AD is complicated, involving the activation of inflammatory immune cells including T helper 2 cells, eosinophils, and macrophages. This activation results in the secretion of various proinflammatory cytokines. Although topical therapeutics is currently used for AD treatment, understanding the pathogenesis of AD is crucial for the development of more effective therapeutics and diagnostics. Therefore, efforts have been made to understand the pathogenesis of AD in order to develop better medications with new paradigms to prevent and treat AD.
Inflammation is a complex immune response that is mediated by inflammatory immune cells to protect the body from invading pathogens, including bacteria, viruses, fungi, and protozoa. It is characterized by several hallmark signs, including redness, swelling, heat, pain, and organ dysfunction [12–14]. Inflammation is a host defense mechanism; however, chronic inflammation is one of the major causes for a variety of human inflammatory and autoimmune diseases [15, 16]. Inflammatory responses are generally induced by innate immune cells, such as monocytes and macrophages, through activating intracellular inflammatory signaling cascades [16–20]. However, a number of studies have reported that inflammatory responses during AD pathogenesis are initiated through the activation of T helper 2 responses due to a breakdown in the balance between T helper 1 and 2 responses [1, 21]. The...