{"title":"Psoriasis Relapse: Exploring the Role of Epigenetics, Metabolic Reprogramming, and Inflammatory Memory.","authors":"Sakshi Wadhavane, Arulkumaran Rithvik, Mahaboobkhan Rasool","doi":"10.1080/08820139.2025.2519666","DOIUrl":null,"url":null,"abstract":"<p><p><b>Background:</b> Psoriasis is a chronic autoimmune condition characterized by recurrent episodes of skin inflammation. Despite progress in treatment, managing flare-ups of psoriasis remains a significant hurdle once the therapy is halted. This review aims to unravel the enigma of relapse by examining the interactions between epigenetics, metabolic reprogramming, and inflammatory memory.<b>Methods and Results:</b> Skin-resident memory T cells and keratinocytes with a history of inflammation play crucial roles in the metabolic and epigenetic alterations observed during relapse. This review explores epigenetic factors involved in the recurrence of psoriasis, such as histone alterations, chromatin restructuring, and non-coding RNAs. Furthermore, we explored environmental influences, metabolic reprogramming, and genetic predispositions that influence the persistence and recurrence of psoriasis. We also outline the function of the gut-brain-skin axis in this scenario. Finally, we discuss pharmacological strategies for managing psoriasis relapse, including targeted biologics.<b>Conclusion:</b> This review provides a comprehensive summary on the intricate epigenetic, molecular, metabolic and environmental cues that exacerbate or facilitate psoriasis relapse. In summary, it also provides an enticing update on the therapeutics currently employed to treat psoriasis relapse.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-27"},"PeriodicalIF":2.9000,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunological Investigations","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/08820139.2025.2519666","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Psoriasis is a chronic autoimmune condition characterized by recurrent episodes of skin inflammation. Despite progress in treatment, managing flare-ups of psoriasis remains a significant hurdle once the therapy is halted. This review aims to unravel the enigma of relapse by examining the interactions between epigenetics, metabolic reprogramming, and inflammatory memory.Methods and Results: Skin-resident memory T cells and keratinocytes with a history of inflammation play crucial roles in the metabolic and epigenetic alterations observed during relapse. This review explores epigenetic factors involved in the recurrence of psoriasis, such as histone alterations, chromatin restructuring, and non-coding RNAs. Furthermore, we explored environmental influences, metabolic reprogramming, and genetic predispositions that influence the persistence and recurrence of psoriasis. We also outline the function of the gut-brain-skin axis in this scenario. Finally, we discuss pharmacological strategies for managing psoriasis relapse, including targeted biologics.Conclusion: This review provides a comprehensive summary on the intricate epigenetic, molecular, metabolic and environmental cues that exacerbate or facilitate psoriasis relapse. In summary, it also provides an enticing update on the therapeutics currently employed to treat psoriasis relapse.
期刊介绍:
Disseminating immunological developments on a worldwide basis, Immunological Investigations encompasses all facets of fundamental and applied immunology, including immunohematology and the study of allergies. This journal provides information presented in the form of original research articles and book reviews, giving a truly in-depth examination of the latest advances in molecular and cellular immunology.