The pathophysiology of atopic eczema.
Atopic eczema (AE) represents a pruritic chronic inflammatory skin disease with a complex background, triggered by genetic and environmental factors. Different dendritic cells subtypes, such as Langerhans cells, inflammatory dendritic epidermal cells and plasmacytoid dendritic cells, play a key role in AE and impact on the mechanisms underlying AE, such as the recruitment of inflammatory cells, T-cell priming, and cytokine and chemokine release. In addition, allergens in combination with bacterial and viral stimuli influence the course and severity of AE. In this review, we highlight the recent progress made in the pathophysiology of AE focusing on the latest research results published in this field.
Allam
J-P
JP
Department of Dermatology, Friedrich-Wilhelms-University, Bonn, Germany.
Novak
N
N
D000938:Antigen-Presenting Cells / Q000276:immunology; D018925:Chemokines / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology*; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D007111:Immunity, Cellular; D011110:Polymorphism, Genetic / Q000235:genetics; D017455:Receptors, IgE / Q000276:immunology; D012867:Skin / Q000276:immunology / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D018925:Chemokines; D016207:Cytokines; D017455:Receptors, IgE