Clinical meaning
The epidermis is a self-renewing stratified squamous epithelium that serves as the primary defensive barrier against mechanical, chemical, microbial, and UV threats. Complete epidermal turnover occurs every 28-30 days through a tightly regulated process of keratinocyte proliferation, differentiation, and desquamation.
Four principal cell types comprise the epidermis: Keratinocytes (90-95%) produce keratin intermediate filaments that provide mechanical strength and assemble the cornified envelope during terminal differentiation. Melanocytes (5-10%) in the stratum basale synthesize melanin within melanosomes, transferring pigment to surrounding keratinocytes via dendritic processes for UV photoprotection. Langerhans cells (3-5%) are bone marrow-derived dendritic antigen-presenting cells (APCs) that sample the epidermal microenvironment, process antigens via MHC class II molecules, and migrate to regional lymph nodes to activate naive T cells. Merkel cells are mechanoreceptors at the dermal-epidermal junction providing fine touch and pressure sensation.
The epidermis is organized into five layers (deep to superficial): stratum basale (single layer of mitotically active keratinocytes anchored to basement membrane by hemidesmosomes), stratum spinosum (polyhedral cells connected by desmosomes, site of Langerhans cell activity), stratum granulosum (keratohyalin granules containing profilaggrin and lamellar bodies releasing lipid bilayers), stratum lucidum (only in thick skin of palms/soles), and stratum corneum (15-30 layers of anucleated corneocytes embedded in lipid matrix - the primary permeability barrier).
Atopic dermatitis (AD) is a chronic inflammatory skin disease driven by Th2-dominant immune dysregulation and epidermal barrier dysfunction. Loss-of-function mutations in filaggrin (FLG gene) are the strongest known genetic risk factor - filaggrin is essential for keratinocyte terminal differentiation and formation of natural moisturizing factor (NMF). Barrier dysfunction allows allergen and microbial penetration, triggering Langerhans cell activation and Th2 polarization. Th2 cytokines IL-4, IL-13, and IL-31 suppress filaggrin expression (positive feedback loop), promote IgE class switching in B cells, recruit eosinophils (via IL-5), and stimulate sensory neurons (IL-31 mediates pruritus).