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Pathogenesis of Atopic Dermatitis: Current Paradigm.
Iran J Immunol 2019; 16(2):97-107IJ

Abstract

Atopic dermatitis (AD) is characterized by skin inflammation, barrier dysfunction and chronic pruritus. In this review, recent advances in the pathogenesis of AD are summarized. Clinical efficacy of the anti-IL-4 receptor antibody dupilumab implies that type 2 cytokines IL-4 and IL-13 have pivotal roles in atopic inflammation. The expression of IL-4 and IL-13 as well as type 2 chemokines such as CCL17, CCL22 and CCL26 is increased in the lesional skin of AD. In addition, IL-4 and IL-13 down-regulate the expression of filaggrin in keratinocytes and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce large amounts of thymic stromal lymphopoietin, IL-25 and IL-33, conducing to type 2 immune deviation via OX40L/OX40 signaling. IL-31, produced by type 2 T cells, is a cardinal pruritogenic cytokine. IL-4 and IL-13 also amplify the IL-31-mediated sensory nerve signal. These molecules are particularly important targets for future drug development for AD.

Authors+Show Affiliations

Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31182684

Citation

Furue, Masutaka, et al. "Pathogenesis of Atopic Dermatitis: Current Paradigm." Iranian Journal of Immunology : IJI, vol. 16, no. 2, 2019, pp. 97-107.
Furue M, Ulzii D, Vu YH, et al. Pathogenesis of Atopic Dermatitis: Current Paradigm. Iran J Immunol. 2019;16(2):97-107.
Furue, M., Ulzii, D., Vu, Y. H., Tsuji, G., Kido-Nakahara, M., & Nakahara, T. (2019). Pathogenesis of Atopic Dermatitis: Current Paradigm. Iranian Journal of Immunology : IJI, 16(2), pp. 97-107. doi:10.22034/IJI.2019.80253.
Furue M, et al. Pathogenesis of Atopic Dermatitis: Current Paradigm. Iran J Immunol. 2019;16(2):97-107. PubMed PMID: 31182684.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathogenesis of Atopic Dermatitis: Current Paradigm. AU - Furue,Masutaka, AU - Ulzii,Dugarmaa, AU - Vu,Yen Hai, AU - Tsuji,Gaku, AU - Kido-Nakahara,Makiko, AU - Nakahara,Takeshi, PY - 2019/6/12/entrez PY - 2019/6/12/pubmed PY - 2019/12/18/medline SP - 97 EP - 107 JF - Iranian journal of immunology : IJI JO - Iran J Immunol VL - 16 IS - 2 N2 - Atopic dermatitis (AD) is characterized by skin inflammation, barrier dysfunction and chronic pruritus. In this review, recent advances in the pathogenesis of AD are summarized. Clinical efficacy of the anti-IL-4 receptor antibody dupilumab implies that type 2 cytokines IL-4 and IL-13 have pivotal roles in atopic inflammation. The expression of IL-4 and IL-13 as well as type 2 chemokines such as CCL17, CCL22 and CCL26 is increased in the lesional skin of AD. In addition, IL-4 and IL-13 down-regulate the expression of filaggrin in keratinocytes and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce large amounts of thymic stromal lymphopoietin, IL-25 and IL-33, conducing to type 2 immune deviation via OX40L/OX40 signaling. IL-31, produced by type 2 T cells, is a cardinal pruritogenic cytokine. IL-4 and IL-13 also amplify the IL-31-mediated sensory nerve signal. These molecules are particularly important targets for future drug development for AD. SN - 1735-367X UR - https://www.unboundmedicine.com/medline/citation/31182684/Pathogenesis_of_Atopic_Dermatitis:_Current_Paradigm DB - PRIME DP - Unbound Medicine ER -