Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies

Psoriasis is a common chronic inflammatory skin disease, associated with substantial comorbidity. TH17 lymphocytes, differentiating under the influence of dendritic cell-derived IL-23, and mediating their effects via IL-17A, are believed to be central effector cells in psoriasis. This concept is und...

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Main Authors: Nicolo Costantino Brembilla, Wolf-Henning Boehncke
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-05-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2023.1186455/full
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author Nicolo Costantino Brembilla
Wolf-Henning Boehncke
Wolf-Henning Boehncke
author_facet Nicolo Costantino Brembilla
Wolf-Henning Boehncke
Wolf-Henning Boehncke
author_sort Nicolo Costantino Brembilla
collection DOAJ
description Psoriasis is a common chronic inflammatory skin disease, associated with substantial comorbidity. TH17 lymphocytes, differentiating under the influence of dendritic cell-derived IL-23, and mediating their effects via IL-17A, are believed to be central effector cells in psoriasis. This concept is underlined by the unprecedented efficacy of therapeutics targeting this pathogenetic axis. In recent years, numerous observations made it necessary to revisit and refine this simple “linear” pathogenetic model. It became evident that IL-23 independent cells exist that produce IL-17A, that IL-17 homologues may exhibit synergistic biological effects, and that the blockade of IL-17A alone is clinically less effective compared to the inhibition of several IL-17 homologues. In this review, we will summarize the current knowledge around IL-17A and its five currently known homologues, namely IL-17B, IL-17C, IL-17D, IL-17E (also known as IL-25) and IL-17F, in relation to skin inflammation in general and psoriasis in particular. We will also re-visit the above-mentioned observations and integrate them into a more comprehensive pathogenetic model. This may help to appreciate current as well as developing anti-psoriatic therapies and to prioritize the selection of future drugs’ mode(s) of action.
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spelling doaj.art-3274fa7e5b1b44b5b415d9f2cb7ad6e72023-05-22T04:50:49ZengFrontiers Media S.A.Frontiers in Immunology1664-32242023-05-011410.3389/fimmu.2023.11864551186455Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapiesNicolo Costantino Brembilla0Wolf-Henning Boehncke1Wolf-Henning Boehncke2Divison of Dermatology and Venereology, Geneva University Hospitals, Geneva, SwitzerlandDivison of Dermatology and Venereology, Geneva University Hospitals, Geneva, SwitzerlandDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, SwitzerlandPsoriasis is a common chronic inflammatory skin disease, associated with substantial comorbidity. TH17 lymphocytes, differentiating under the influence of dendritic cell-derived IL-23, and mediating their effects via IL-17A, are believed to be central effector cells in psoriasis. This concept is underlined by the unprecedented efficacy of therapeutics targeting this pathogenetic axis. In recent years, numerous observations made it necessary to revisit and refine this simple “linear” pathogenetic model. It became evident that IL-23 independent cells exist that produce IL-17A, that IL-17 homologues may exhibit synergistic biological effects, and that the blockade of IL-17A alone is clinically less effective compared to the inhibition of several IL-17 homologues. In this review, we will summarize the current knowledge around IL-17A and its five currently known homologues, namely IL-17B, IL-17C, IL-17D, IL-17E (also known as IL-25) and IL-17F, in relation to skin inflammation in general and psoriasis in particular. We will also re-visit the above-mentioned observations and integrate them into a more comprehensive pathogenetic model. This may help to appreciate current as well as developing anti-psoriatic therapies and to prioritize the selection of future drugs’ mode(s) of action.https://www.frontiersin.org/articles/10.3389/fimmu.2023.1186455/fullpsoriasispsoriatic arthritisIL-17IL-25TH17 cellsTYK2
spellingShingle Nicolo Costantino Brembilla
Wolf-Henning Boehncke
Wolf-Henning Boehncke
Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies
Frontiers in Immunology
psoriasis
psoriatic arthritis
IL-17
IL-25
TH17 cells
TYK2
title Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies
title_full Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies
title_fullStr Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies
title_full_unstemmed Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies
title_short Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies
title_sort revisiting the interleukin 17 family of cytokines in psoriasis pathogenesis and potential targets for innovative therapies
topic psoriasis
psoriatic arthritis
IL-17
IL-25
TH17 cells
TYK2
url https://www.frontiersin.org/articles/10.3389/fimmu.2023.1186455/full
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