Journal
JOURNAL OF PHARMACOLOGICAL SCIENCES
Volume 110, Issue 3, Pages 232-236Publisher
JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1254/jphs.09R02FM
Keywords
atopic dermatitis; nonatopic dermatitis; barrier dysfunction; filaggrin; IgE autoantibody; allergic inflammation
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It has been recognized that atopic dermatitis (AD) involves allergen-driven Th2 cell polarization. In patients with AD, cytokines induce allergic inflammatory responses and subsequently enhance IgE production. Recent reports revealed that a reduced barrier function as well as altered immunity are fundamental to the development of AD because barrier disruption due to aberrant Filaggrin expression is a pathological factor. However, although recent Studies have improved our understanding of the pathogenesis of AD, the overall pathophysiology remains elusive. I herein discuss it based on the natural history of AD.
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