Abstract
The immunology of eczema involves an interaction of adaptive and innate immune responses. Toll-like receptor 2 (TLR2) activity drives the reaction that ultimately results in an eczematous lesion. Pathways leading towards inflammatory responses include the MyD88 pathway, which can be set in motion by nearly all the cells in the epidermis. This pathway leads to nuclear factor-κB, which mediates inflammation in part by the production of tumor necrosis factor α (TNFα). TNFα is considered the most important mediator of spongiosis, which is the leading pathological finding. Also important is the stimulation by TLR2 of PAR2 (protease-activating receptor 2), the molecule that is the leading pruritogen in eczema.
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References
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Allen, H.B. (2015). Immunology. In: The Etiology of Atopic Dermatitis. Springer, London. https://doi.org/10.1007/978-1-4471-6545-3_4
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DOI: https://doi.org/10.1007/978-1-4471-6545-3_4
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