Th17 cells and tissue remodeling in atopic and contact dermatitis

Simon, Dagmar; Aeberhard, Carla; Erdemoglu, Y.; Simon, Hans Uwe

doi:10.1111/all.12351

Cited by 63 publications

(45 citation statements)

References 58 publications

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“…IL-33 produced by keratinocytes may also stimulate group 2 innate lymphoid cells that produce abundant Th2 cytokines including IL-5 and IL-13 [102]. In addition to Th2 responses, Th1, Th17, and Th22 cells and their corresponding cytokines have been detected in AD skin, suggesting possible roles, e.g., in evoking spongiosis [103], for the induction of antimicrobial peptide production [104] or in stimulation of epidermal hyperplasia and remodeling [105, 106]. Interestingly, Asian AD patients have been reported to exhibit a distinct phenotype with Th2 skewing and Th17 polarization [8].…”

Section: Pathogenenic Mechanismsmentioning

confidence: 99%

Atopic Dermatitis: Collegium Internationale Allergologicum (CIA) Update 2019

Simon

Wollenberg

Renz

et al. 2019

Int Arch Allergy Immunol

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Atopic dermatitis (AD) is a chronic inflammatory skin disease presenting with recurrent eczematous lesions and intense pruritus. It is common and affects both children and adults, often beginning in infancy. Due to the unpredictable disease course, its visible skin lesions, itching and scratching followed by sleeplessness, other associated atopic diseases, and behavioral and psychiatric disorders, AD is an immense burden for patients and caregivers. AD is determined by a genetic predisposition characterized by an impaired skin barrier and a T-helper-2-predominant inflammation. Restoration of the skin barrier is the main approach for treating and preventing AD. In order to cope with acute flares, usually topical corticosteroids (TCS) are applied, while topical calcineurin inhibitors (TCI) are used mainly for maintenance therapy. There is a small group of patients who are refractory to TCS and TCI and require systemic immunosuppressive drugs such as ciclosporin. Novel, targeted therapies are under clinical investigation, among which an anti-IL-4/IL-13 receptor antibody has recently been approved in several countries. As we learn to understand the pathomechanisms of AD, the characteristics of the different patient subgroups, and the effectiveness of various targeted therapies, a personalized treatment ensuring the best efficacy and safety and, probably, a disease-modifying effect will result.

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Section: Pathogenenic Mechanismsmentioning

confidence: 99%

Atopic Dermatitis: Collegium Internationale Allergologicum (CIA) Update 2019

Simon

Wollenberg

Renz

et al. 2019

Int Arch Allergy Immunol

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“…Kronik lezyonlardaki hücresel infiltratta Th2 ile birlikte, interferon (IFN)ɣ ve IL-12 üreten Th1 hücreleri ve akut lezyonlardan daha az oranda olmak üzere Th22 ve Th17 bulunur 18,19 . Th17 ve Th22, timik stromal limfopoetin gibi keratinosit ve fibroblastlardan salınan sitokin ve kemokinlerle birlikte dokunun yeniden yapılandırmasını ve fibrozisini gerçekleştirirler [18][19][20][21] . AD'de dermal dentritik hücrelerden başka, trimerik yüksek affiniteli IgE reseptörü taşıyan epidermal Langerhans hücreleri ve enflamatuvar dentritik hücreler de antijen sunumunda görev alır.…”

Section: Deri Enflamasyonuunclassified

The Turkish guideline for the diagnosis and management of atopic dermatitis-2018

Ertam¹,

Küçük²,

Alper³

et al. 2018

TURKDERM

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“…Ра-нее было продемонстрировано, что экспрессия ИЛ-17 и ИЛ-22 связана с защитной функцией кожи, в частности, с синтезом антимикробных пептидов [102]. Известно, что ИЛ-23 стимулирует дифференцировку и пролиферацию Т-клеток в Th17, которые в свою очередь продуцируют ИЛ-17.…”

Section: антицитокиновая терапияunclassified

Biological Therapeutic Treatment of Atopic Dermatitis

Кубанова

Кубанов

Карамова

et al. 2017

Vestnik dermatologii i venerologii

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Atopic dermatitis is a chronic recurrent inflammatory disease caused, inter alia, by violations of the barrier function of the skin and pathological immune response in the form of an imbalance of Th1 and Th2 lymphocytes with increased production of IL-4, IL-5, IL-13, IL-31. Treatment of severe forms of atopic dermatitis is not an easy task due to the variability of the individual response to treatment, the short duration of the therapeutic effect and the frequent development of undesirable phenomena associated with the use of existing methods of systemic immunosuppressive therapy. The study of the pathogenesis of atopic dermatitis made it possible to identify the spectrum of molecular targets, providing the basis for researching alternative variants to the previously used systemic therapy methods – genetic engineering biological preparations. Contemporary data on the pathogenesis of atopic dermatitis as well as potential molecular targets for innovative biological preparations, the efficacy of which has been evaluated through clinical trials, are presented in the review.

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Th17 cells and tissue remodeling in atopic and contact dermatitis

Abstract: The expression of IL-17 and related cytokines, such as IL-22, was demonstrated in acute eczematous lesions independent of their pathogenesis. Our results suggest a potential role for IL-17 in remodeling of the skin.

Cited by 63 publications

References 58 publications

Atopic Dermatitis: Collegium Internationale Allergologicum (CIA) Update 2019

Atopic Dermatitis: Collegium Internationale Allergologicum (CIA) Update 2019

The Turkish guideline for the diagnosis and management of atopic dermatitis-2018

Biological Therapeutic Treatment of Atopic Dermatitis

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