Targeting interleukin 4 receptor alpha in atopic dermatitis - focus on pre-clinical models. Hadebe, S & Brombacher, F. Current Allergy and Clinical Immunology, 35(2):82–86, 2022.
doi  abstract   bibtex   
Skin is the largest organ of the human body, which means it is in the first line of defence in protecting its host from external agents such as bacteria, fungi, viruses and other infectious agents. What shapes a healthy skin micro-environment is direct contact of skin-resident commensals with structural cells such as keratinocytes and resident immune cells that help maintain the integrity of the barrier. Environmental stressors can dysregulate this tightly regulated balance between skin-resident microbiota and immune cells that protect the skin, causing aberrant inflammatory conditions. Genetic predisposition is another factor that influences this skin-microbiota dysregulation and it is observed in conditions such as atopic dermatitis (AD) or psoriasis. How immune cells help maintain this skin barrier is of significant interest, particularly for therapies that may be directed at the host. Recent studies put Type-2 immunity at the centre in immune-cell-driven skin resolution, repair after injury and pathogenesis during immune dysregulation. Interleukin receptor alpha (IL-4R$α$) is central to Type-2 immunity and is a target for many inflammatory conditions of the skin, such as AD. In this review, we discuss IL-4R$α$ immunity, genetics and signalling in the context of pre-clinical models of AD.
@article{Hadebe2022,
abstract = {Skin is the largest organ of the human body, which means it is in the first line of defence in protecting its host from external agents such as bacteria, fungi, viruses and other infectious agents. What shapes a healthy skin micro-environment is direct contact of skin-resident commensals with structural cells such as keratinocytes and resident immune cells that help maintain the integrity of the barrier. Environmental stressors can dysregulate this tightly regulated balance between skin-resident microbiota and immune cells that protect the skin, causing aberrant inflammatory conditions. Genetic predisposition is another factor that influences this skin-microbiota dysregulation and it is observed in conditions such as atopic dermatitis (AD) or psoriasis. How immune cells help maintain this skin barrier is of significant interest, particularly for therapies that may be directed at the host. Recent studies put Type-2 immunity at the centre in immune-cell-driven skin resolution, repair after injury and pathogenesis during immune dysregulation. Interleukin receptor alpha (IL-4R$\alpha$) is central to Type-2 immunity and is a target for many inflammatory conditions of the skin, such as AD. In this review, we discuss IL-4R$\alpha$ immunity, genetics and signalling in the context of pre-clinical models of AD.},
author = {Hadebe, S and Brombacher, Frank},
doi = {10.520/ejc-caci-v35-n2-a6},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Hadebe, Brombacher - 2022 - Targeting interleukin 4 receptor alpha in atopic dermatitis - focus on pre-clinical models.pdf:pdf},
journal = {Current Allergy and Clinical Immunology},
keywords = {OA,fund{\_}ack,review},
mendeley-tags = {OA,fund{\_}ack,review},
number = {2},
pages = {82--86},
title = {{Targeting interleukin 4 receptor alpha in atopic dermatitis - focus on pre-clinical models}},
volume = {35},
year = {2022}
}

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