2018
DOI: 10.1016/j.jid.2018.05.001
|View full text |Cite
|
Sign up to set email alerts
|

Psoriasis Plays a Wild CARD

Abstract: Rare autosomal mutations in CARD14 have previously been linked to psoriasis susceptibility in humans, but their pathogenic role had not been shown. Mellett et al. generated mice harboring the patient-derived gain-of-function Card14ΔE138 mutation and showed that hyperactivation of CARD14 alone is sufficient to induce immunopathogenic mechanisms that are responsible for psoriasis, which is driven by the IL-17/IL-23 axis.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

0
3
0

Year Published

2020
2020
2022
2022

Publication Types

Select...
3

Relationship

0
3

Authors

Journals

citations
Cited by 3 publications
(3 citation statements)
references
References 10 publications
0
3
0
Order By: Relevance
“…This is not surprising given the overlapping genetics of PRP and psoriasis, including CARD14 mutations, which are associated with familial and sporadic PRP and induce psoriasiform skin inflammation in mice mediated by the IL-23/IL-17 pathway. 25,26 One PRP patient in our cohort had a confirmed CARD14 mutation and improved with ustekinumab. 24 These data indicate that IL-36 staining cannot be used to differentiate between PRP and psoriasis in cases with overlapping histopathologic features.…”
Section: Discussionmentioning
confidence: 88%
“…This is not surprising given the overlapping genetics of PRP and psoriasis, including CARD14 mutations, which are associated with familial and sporadic PRP and induce psoriasiform skin inflammation in mice mediated by the IL-23/IL-17 pathway. 25,26 One PRP patient in our cohort had a confirmed CARD14 mutation and improved with ustekinumab. 24 These data indicate that IL-36 staining cannot be used to differentiate between PRP and psoriasis in cases with overlapping histopathologic features.…”
Section: Discussionmentioning
confidence: 88%
“…Previously, the association of CARD14 variants with psoriasis was reported in Japanese [ 33 ], Spanish [ 34 ], European [ 35 ], Chinese [ 31 , 32 , 36 , 37 ], and Tunisian [ 38 ] populations. Mechanistically, the mutations in the CARD14 gene lead to hyperinflammation in the keratinocytes, which causes immune cell infiltration, hyperproliferation of keratinocytes, and keratosis, which are typical hallmarks of psoriasis [ 39 ]. An in vivo study by Mellett et al [ 40 ] provided significant insights into the disease mechanism driven by CARD14 gain of function mutations.…”
Section: Discussionmentioning
confidence: 99%
“…Psoriasis has evolved conceptually over time, from being considered a skin disease in its first descriptions, currently we can define it as a chronic and inflammatory skin disease, without a defined, genetically determined, pathophysiologically autoimmune etiology, of intermittent evolution, at risk of skin, systemic and psychological comorbidities, which impact on quality of life [1]. The most characteristic feature of psoriasis is the hyperproliferation and altered differentiation of keratinocytes, in addition to immune, biochemical, and vascular abnormalities influenced by multiple environmental factors that can trigger or exacerbate its evolution, affecting between 2 and 3% of the population.…”
Section: Introductionmentioning
confidence: 99%