Immunopathologie du psoriasis

Masson, Adèle de; Bouaziz, Jean‐David; Battistella, Maxime; Bagot, Martine; Bensussan, Armand

doi:10.1051/medsci/20163203009

Cited by 9 publications

(5 citation statements)

References 50 publications

(29 reference statements)

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“…Increased frequencies of CD4+ T cells have been consistently discovered in psoriatic skin lesions [ 31 ]. Besides, a role of Th1 CD4 T cells was initially suspected and Th17 CD4 T cells have been shown to play a major role in psoriasis recently [ 32 ]. We queried the biological function for each correlated SNP in functional genomic data sets.…”

Section: Methodsmentioning

confidence: 99%

A catalog of potential putative functional variants in psoriasis genome-wide association regions

et al. 2018

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Psoriasis is a common inflammatory skin disease, with considerable genetic contribution. Genome-wide association studies have successfully identified a number of genomic regions for the risk of psoriasis. However, it is challenging to pinpoint the functional causal variants and then further decipher the genetic mechanisms underlying each region. In order to prioritize potential functional causal variants within psoriasis susceptibility regions, we integrated the genetic association findings and functional genomic data publicly available, i.e. histone modifications in relevant immune cells. We characterized a pervasive enrichment pattern of psoriasis variants in five core histone marks across immune cells/tissues. We discovered that genetic alleles within psoriasis association regions might influence gene expression levels through significantly affecting the binding affinities of 17 transcription factors. We established a catalog of 654 potential functional causal variants for psoriasis and suggested that they significantly overlapped with causal variants for autoimmune diseases. We identified potential causal variant rs79824801 overlay with the peaks of five histone marks in primary CD4+ T cells. Its alternative allele affected the binding affinity of transcription factor IKZF1. This study highlights the complex genetic architecture and complicated mechanisms for psoriasis. The findings will inform the functional experiment design for psoriasis.

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Section: Methodsmentioning

confidence: 99%

A catalog of potential putative functional variants in psoriasis genome-wide association regions

et al. 2018

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“…Le diagnostic d'arthrite goutteuse, en l'absence de ponction articulaire et de preuve microscopique, est parfois incertain. Lorsque le patient est inclassable, une observation détaillée permettra une meilleure dissection entre les possibles entités (goutte ou psoriasis) [27]…”

Section: Les Rhumatismes Impursunclassified

Quelle taxonomie des maladies inflammatoires en rhumatologie ?

et al. 2021

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La pratique clinique de la médecine nécessite la reconnaissance de la maladie dont souffre le patient par le médecin. Pour cela, celui-ci rationnalise les signes permettant d’isoler une entité réaliste et de la classer dans la nosologie de référence. Contrairement à d’autres pratiques, le modèle biomédical utilise la méthodologie scientifique du recensement, dans une logique de classification pour définir les maladies. Du fait de son processus de simplification, ce modèle néglige les cas de transition ou les cas complexes. En rhumatologie, ce raisonnement classifiant est mis à l’épreuve par le manque d’objectivité et de spécificité des éléments sur lesquels s’appuie le clinicien pour construire le diagnostic, mais aussi par la complexité des mécanismes physiopathologiques des maladies rhumatismales. Ces maladies peuvent en effet se confondre ou s’intriquer, pour aboutir alors à la description de nouvelles entités non envisagées dans les classifications. Nous présentons dans cette revue les difficultés rencontrées au cours de l’exercice de la médecine dans ces contextes, et comment, à partir d’un cas concret, vécu, celles-ci peuvent donner naissance à la proposition d’un nouveau taxon1.

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“…All these mediators further maintain keratinocytes activation producing the now so-called auto-antigen, LL-37, proinflammatory cytokines (TNF-α, IL-1β, IL-6), chemokines and S100 proteins, propagating the chronic inflammation [20]. Altogether, these promote keratinocyte proliferation, production of AMPs and chemokines which promote neutrophil recruitment and sustain skin inflammation (Figure 1) [12,21,22,23,24].…”

Section: Psoriasis Pathogenesis In Briefmentioning

confidence: 99%

Advances in Understanding the Immunological Pathways in Psoriasis

Georgescu

Tampa

Căruntu

et al. 2019

IJMS

113

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Psoriasis vulgaris is a chronic, immune-mediated, inflammatory, polygenic skin disorder affecting approximately 2% of the population. It has a great impact on quality of life; patients often experience depression, anxiety, stigma as well as suicidal behavior. Even though psoriasis is one of the most studied dermatological conditions, the pathogenesis of the disease is still not completely elucidated. The complex interactions between keratinocytes, dendritic cells, T-lymphocytes, neutrophils and mast cells are responsible for the histopathological changes seen in psoriasis. The pathogenic model leading to the formation of psoriatic plaques has however evolved a lot over the years. There is now enough evidence to support the role of interleukin (IL) -23, IL-17, IL-22, T helper (Th) -17 cells, Th-22 cells, T regulatory cells, transforming growth factor (TGF)-β1 and IL-10 in the pathogenesis of the disease. Moreover, several inflammatory and anti-inflammatory molecules are currently being investigated, some of them showing promising results. The aim of this paper is to look over the most recent advances in the immunological pathways involved in the pathogenesis of psoriasis vulgaris.

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Immunopathologie du psoriasis

Cited by 9 publications

References 50 publications

A catalog of potential putative functional variants in psoriasis genome-wide association regions

A catalog of potential putative functional variants in psoriasis genome-wide association regions

Quelle taxonomie des maladies inflammatoires en rhumatologie ?

Advances in Understanding the Immunological Pathways in Psoriasis

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