Atopic dermatitis is a common skin disorder with a complex, evolving pathogenesis. Research on the pathogenesis has shifted from focusing primarily on generalized immune system abnormalities in T helper 1/T helper 2 (TH1/TH2) activity to more targeted immune and skin barrier abnormalities contributing to the overall phenotype. Specific signaling pathways recently implicated in atopic dermatitis include production of interleukin (IL) 4 and IL-13, which promote immunoglobulin E production, TH17 and TH22 cells, and production of cytokines. Barrier defect abnormalities, such as a shared filaggrin mutation noted in ichthyosis vulgaris and atopic dermatitis, as well as reduced structural proteins and lipids (eg, ceramides), have been discovered as well. These alterations contribute to increased transepidermal water loss in addition to increased allergen exposure, resulting in debate over the “inside out” versus “outside in” theories—that is, the concept that immunity triggers barrier breakdown versus barrier abnormalities triggering immunologic alteration toward atopy. In fact, it is likely that all of these contribute to pathogenesis, with some individuals initially experiencing immunologic abnormalities more strongly than barrier defects and vice versa. Genetic analyses have continued to advance, leading to the discovery of potential candidate genes relating both to the impaired skin barrier and the altered immune system pathways. This review outlines the evolution of the field of current pathogenesis of atopic dermatitis, highlighting the most pertinent recent findings.
|Number of pages||5|
|Journal||Clinics in Dermatology|
|State||Published - 1 Jul 2017|