This document discusses the pathophysiology of atopic dermatitis. It describes how a filaggrin mutation can disrupt the skin barrier, allowing allergens to enter and be captured by Langerhans cells or mast cells in individuals with an atopic tendency. This leads to either a T cell-mediated delayed hypersensitivity reaction through Th1 and Th2 differentiation, or an IgE-mediated immediate hypersensitivity reaction through mast cell degranulation and release of inflammatory factors.
This document discusses the pathophysiology of atopic dermatitis. It describes how a filaggrin mutation can disrupt the skin barrier, allowing allergens to enter and be captured by Langerhans cells or mast cells in individuals with an atopic tendency. This leads to either a T cell-mediated delayed hypersensitivity reaction through Th1 and Th2 differentiation, or an IgE-mediated immediate hypersensitivity reaction through mast cell degranulation and release of inflammatory factors.
This document discusses the pathophysiology of atopic dermatitis. It describes how a filaggrin mutation can disrupt the skin barrier, allowing allergens to enter and be captured by Langerhans cells or mast cells in individuals with an atopic tendency. This leads to either a T cell-mediated delayed hypersensitivity reaction through Th1 and Th2 differentiation, or an IgE-mediated immediate hypersensitivity reaction through mast cell degranulation and release of inflammatory factors.
antigen exposure in individuals with atopic tendency Presenting to peripheral lymph node differentiation of naive T cell Cooperate with MHC II Th 1 : IFN-, TNF, IL-2, IL-17 Th 2: IL-4, IL-5, IL-13
T cell mediated, delayed type
hypersensitivity Disruption of skin barrier Filaggrin mutation
Captured by IgE on the
surface of mast cell antigen exposure in individuals with atopic tendency Cross-linking between IgE and FceR Degranulation of mast cell releasing histamine and others chemotactic factors