Interactions between the immune system

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Atopic dermatitis Pathophysiology Atopic dermatitis (AD), or eczema, is a chronic, relapsing inflammatory skin disease with a prevalence of up to 25% in children and 7% in adults (10). Symptoms beginning in childhood may subside in adolescence or continue for years, involving periods of exacerbation and remission. Affected individuals have dry, cracked skin, intense pruritus and a erythematous rash due to Th2 immune responses against allergens (Figure 1). The skin barrier is impaired within crusted erythematous areas, associated with epidermal hyperplasia, scaling and lichenification (10). Some individuals have deficiencies in filaggrin or antimicrobial peptides, increasing permeability of the skin and susceptibility to opportunistic infections, respectively.

During infancy, atopic sensitization is also associated with IL9, IL33 and IL33R expression. Scratching affected regions leads to further impairment of the epidermal barrier, increasing susceptibility to opportunistic pathogens including Spain phone number list Staphylococcus aureus. Figure 1 www.frontiersin FIGURE 1. A microbiome in atopic dermatitis. In healthy individuals, the epidermal barrier is intact and maintained by filaggrin expression, antimicrobial peptides, and other factors. This is associated with a diverse microbiome that colonizes distinct niches on the skin surface.



Atopic dermatitis (AD) patients have an impaired skin barrier leading to increased permeability within the keratinocyte layers. This is associated with reduced microbial diversity, including increased colonization with Staphylococcus aureus. These individuals are at increased risk of inflammatory skin injury, leading to the production of cytokines that facilitate Th2 cell differentiation. Allergen-specific Th2 cells then produce cytokines that promote eosinophil recruitment to the skin and IgE production by B cells. Mast cells that are sensitized with IgE release histamine and other inflammatory mediators following subsequent exposures to the skin allergen, while eosinophils mediate skin damage by releasing intracellular granules.