Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis : A molecular insight
Copyright © 2018 Elsevier Inc. All rights reserved.
| Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 206(2019) vom: 01. Sept., Seite 15-22 |
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| Auteur principal: | |
| Autres auteurs: | , , , |
| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2019
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| Accès à la collection: | Clinical immunology (Orlando, Fla.) |
| Sujets: | Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review Cytokines Human monoclonal IL-23 antibodies IL-23/IL-23R pathways Psoriatic arthritis Skin and joint inflammation Therapeutics plus... |
| Résumé: | Copyright © 2018 Elsevier Inc. All rights reserved. Psoriatic arthritis (PsA) is a chronic inflammatory arthritis of unknown etiology, and currently the cellular and molecular interactions that dictate its pathogenesis remain elusive. A role of the interleukin-23 (IL-23)/IL-23R (IL-23 receptor) interaction in the development of psoriasis and PsA is well established. As IL-23 regulates the differentiation and activation of innate and adaptive immunity, it pertains to a very complex pathophysiology involving a plethora of effectors and transducers. In this review, we will discuss recent advances on the cellular and molecular pathophysiological mechanisms that regulate the initiation and progression of PsA as well as new therapeutic approaches for IL-23/IL-23R targeted therapeutics |
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| Description: | Date Completed 11.05.2020 Date Revised 10.04.2022 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2018.09.002 |