The Inside-Out View

According to the inside-out theory, genetic factors predispose patients with atopic dermatitis to develop abnormally high numbers of type 2 helper T cells (TH2). Allergens are initially encountered by dendritic cells that then migrate into the dermis. These dendritic cells then stimulate naive T cells to become TH2 cells, which produce the proinflammatory allergic cytokines (IL-4, IL-5 and IL-13), and stimulate B cells to produce antigen-specific IgE (see the "Initial" stage in the figure below). Increased IgE in response to allergen exposure activates mast cell, which further stimulate secretion of a variety of inflammatory mediators. These mediators collectively further increase vascular permeability, vasodilation, and inflammation. (see the "Early" stage in the figure below). Ongoing inflammation is aggravated by hypersensitivity to foods and aeroallergens.

Increased production of IL-4, 5 and 13 decreases production of ceramides, filaggrin, and antimicrobial peptides. These changes in turn further compromises the skin barrier, worsens hydration and compromises antimicrobial defence completing the "Inside-Out" pathogeneses of atopic dermatitis.

Diagram of the Inside-Out View of Atopic Dermatitis

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