The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis
Psoriasis (Ps) and psoriatic arthritis (PsA) represent a clinical and immunopathogenic continuum, called psoriatic disease, cumulatively affecting approximately 3% of the general population. Psoriatic disease is a chronic inflammatory disorder affecting the skin and musculoskeletal system. The immun...
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doaj-2a7eed4f39f94bfe950974d41dd28b7a2021-07-14T11:35:21ZengSAGE PublishingTherapeutic Advances in Musculoskeletal Disease1759-72182019-11-011110.1177/1759720X19886505The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritisLukas FrischknechtMatteo VecellioCarlo SelmiPsoriasis (Ps) and psoriatic arthritis (PsA) represent a clinical and immunopathogenic continuum, called psoriatic disease, cumulatively affecting approximately 3% of the general population. Psoriatic disease is a chronic inflammatory disorder affecting the skin and musculoskeletal system. The immuno-pathogenesis is characterized by an activation of the TNF/IL-23/IL-17 cytokine axis, leading to an immunologic imbalance of T-cells resident in all affected tissues, mainly entheses. In the majority of cases, skin Ps predates rheumatological manifestations. Secondary to the higher incidence and the availability of mouse models, there is stronger data available on skin Ps, and data are, in most cases, relevant also to PsA. In a widely accepted model, environmental trigger factors like infections or trauma are capable of initiating an inflammatory cascade, ultimately creating a sustained state of chronic inflammation in genetically susceptible individuals. Besides well-known genetic susceptibility loci, epigenetic DNA modifications, which are associated with Ps development have been characterized recently and will be discussed in this article. The current evidence is promising in the possibility to provide new therapeutic avenues and fill the unmet need of patients, for whom current treatments either do not allow the disease to be controlled or must be continued for life.https://doi.org/10.1177/1759720X19886505 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lukas Frischknecht Matteo Vecellio Carlo Selmi |
spellingShingle |
Lukas Frischknecht Matteo Vecellio Carlo Selmi The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis Therapeutic Advances in Musculoskeletal Disease |
author_facet |
Lukas Frischknecht Matteo Vecellio Carlo Selmi |
author_sort |
Lukas Frischknecht |
title |
The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis |
title_short |
The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis |
title_full |
The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis |
title_fullStr |
The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis |
title_full_unstemmed |
The role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis |
title_sort |
role of epigenetics and immunological imbalance in the etiopathogenesis of psoriasis and psoriatic arthritis |
publisher |
SAGE Publishing |
series |
Therapeutic Advances in Musculoskeletal Disease |
issn |
1759-7218 |
publishDate |
2019-11-01 |
description |
Psoriasis (Ps) and psoriatic arthritis (PsA) represent a clinical and immunopathogenic continuum, called psoriatic disease, cumulatively affecting approximately 3% of the general population. Psoriatic disease is a chronic inflammatory disorder affecting the skin and musculoskeletal system. The immuno-pathogenesis is characterized by an activation of the TNF/IL-23/IL-17 cytokine axis, leading to an immunologic imbalance of T-cells resident in all affected tissues, mainly entheses. In the majority of cases, skin Ps predates rheumatological manifestations. Secondary to the higher incidence and the availability of mouse models, there is stronger data available on skin Ps, and data are, in most cases, relevant also to PsA. In a widely accepted model, environmental trigger factors like infections or trauma are capable of initiating an inflammatory cascade, ultimately creating a sustained state of chronic inflammation in genetically susceptible individuals. Besides well-known genetic susceptibility loci, epigenetic DNA modifications, which are associated with Ps development have been characterized recently and will be discussed in this article. The current evidence is promising in the possibility to provide new therapeutic avenues and fill the unmet need of patients, for whom current treatments either do not allow the disease to be controlled or must be continued for life. |
url |
https://doi.org/10.1177/1759720X19886505 |
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