Th2 Cytokines and Atopic Dermatitis

By E. Brandt, U. Sivaprasad. Journal of Clinical & Cellular Immunology, 2011

644 citations recorded by the source corpus.

Atopic dermatitis (AD), a chronic relapsing inflammatory skin disease, is increasing in prevalence around the world. Intensive research is ongoing to understand the mechanisms involved in the development of AD and offer new treatment options for patients suffering from AD. In this review, we highlight the importance of allergic Th2 responses in the development of the disease and summarize relevant literature, including genetic studies, studies of human skin and mechanistic studies on keratinocytes and mouse models of AD. We discuss the importance of the skin barrier and review recent findings on the pro-Th2 cytokines TSLP, IL-25, and IL-33, notably their ability to polarize dendritic cells and promote Th2 responses. After a brief update on the contribution of different T-cell subsets to AD, we focus on Th2 cells and the respective contributions of each of the Th2 cytokines (IL-4, IL-13, IL-5, IL-31, and IL-10) to AD. We conclude with a brief discussion of the current gaps in our knowledge and technical limitations.

Subfields: Dermatology, Immunology and Allergy, Rheumatology

View Paper: https://www.semanticscholar.org/paper/a50eabeda19c0cfaa91027d1111a58e4f904889f

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Citations in the corpus

Progressive activation of Th2/Th22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis (2012, background): “Unlike psoriasis, another common inflammatory skin disease that is increasingly considered a TH17 disease and for which an increased understanding of pathogenic mechanisms led to the development of revolutionary targeted therapeutics, the pathogenesis of AD is still enigmatic, resulting in a lack of”
TSLP elicits IL-33–independent innate lymphoid cell responses to promote skin inflammation (2013, background): “AD in humans has been associated with enhanced expression of the predominantly epithelial cell–derived cytokines IL-33, IL-25, and thymic stromal lymphopoietin (TSLP) in the skin, which elicit the TH2 cell– associated cytokine responses that are known to promote disease (14).”