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Getting more and more complex: the pathophysiology of atopic eczema


European Journal of Dermatology. Volume 17, Number 4, 267-83, July-August 2007, Review article

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Author(s) : Laura Maintz, Natalija Novak

Summary : Atopic eczema (AE) is a multifactorial chronic inflammatory skin disease characterized by pruritic, typically distributed eczematous skin lesions. Deficiencies in innate and adaptive immunity based on a genetic predisposition result in skin barrier dysfunction with hyperreactivity to environmental stimuli and susceptibility to skin infections which influence the course and severity of AE. In this review, we provide an overview of the complex pathophysiology of AE with a focus on recent advances published in this field.

Keywords : AE, Atopic eczema, AMP, Antimicrobial peptides, APC, Antigen-presenting cells, BDNF, brain-derived neurotrophic factor, DC, Dendritic cells, pDC, plasmacytoid dendritic cells, DCD, Dermcidin, EDC, Epidermal differentiation complex, EH, Eczema herpeticatum, FLG, Filaggrin gene, GM-CSF, Granulocyte macrophage colony-stimulating factor, HBD, Human β-defensin, IDEC, Inflammatory dendritic epidermal cells, IgE, Immunglobulin E, IL, Interleukin, LC, Langerhans cells, LPS, Lipopolysaccharide, LTA, Lipoteichoic acid, NOD, Nucleotide-binding oligomerization domain, NK, Natural killer cell, NGF, nerve growth factor, NT, Neurotrophin, P75 NTR, Pan-neurotrophin receptor (NTR) p75, PAMP, Pathogen associated molecular pattern, PGN, Peptidoglycan, PRR, Pattern recognition receptor, PAR, Proteinase-activated receptor, RANTES, Regulated upon activation, normally T cell expressed and secreted/CCL5, S. aureus, Staphylococcus aureus, SC, Stratum corneum, SNP, Single nucleotide polymorphism, SP, Serine protease, TARC, Thymus and activation regulated chemokine/CCL17, TG, Transglutaminase, trk, tyrosine kinase receptor, Th, Helper T lymphocyte, TLR, Toll-like receptor, TNF-α, Tumor-necrosis factor (TNF)-α

 

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