Lack of association between CARD10/CARMA3 tag SNPs and psoriasis vulgaris in the southern Chinese population

Shi, Ge; Zhang, M.F.; Liao, Peizhou; Wang, T.T.; Li, S.J.; Fan, Yi‐Ming; Zhu, Kunju

doi:10.4238/gmr16019025

Cited by 3 publications

(2 citation statements)

References 19 publications

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“… 93 Moreover, the CARD10 SNPs were not association with psoriasis in another Chinese population. 94 The rs11652075 CC (p.Arg820Trp) genotype of CARD14 was significantly associated with psoriasis in a Spanish cohort. 95 The CARD14 c.526G > C (p.Asp176His) polymorphism was found to be a significant risk factor for generalized pustular psoriasis in a Japanese cohort.…”

Section: Inflammasome-related Genesmentioning

confidence: 97%

Psoriasis: An Immunogenetic Perspective

Kocaaga

2022

Glob Med Genet

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Psoriasis is an erythematous-squamous dermatosis with a polygenic inheritance history. Both environmental and genetic factors play a role in the etiology of the disease. Over the past two decades, numerous linkage analyzes and genome-wide association studies have been conducted to investigate the role of genetic variation in disease pathogenesis and progression. To date, >70 psoriasis susceptibility loci have been identified, including HLA-Cw6, IL12B, IL23R, and LCE3B/3C. Some genetic markers are used in clinical diagnosis, prognosis, treatment, and personalized new drug development that can further explain the pathogenesis of psoriasis. This review summarizes the immunological mechanisms involved in the etiopathogenesis of psoriasis and recent advances in susceptibility genes and highlights new potential targets for therapeutic intervention.

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Section: Inflammasome-related Genesmentioning

confidence: 97%

Psoriasis: An Immunogenetic Perspective

Kocaaga

2022

Glob Med Genet

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“…Furthermore, the CARD14 gene rs11652075 polymorphism was associated with clinical manifestations of PsV patients [ 56 ]. However, evaluation of seven tag SNPs in the CARMA3/CARD10 gene in 355 patients with PsV and 213 control subjects disclosed no significant association of these SNPs with the disease risk [ 57 ].…”

Section: Psoriasis and Non-mhc Genesmentioning

confidence: 99%

Etiopathogenesis of Psoriasis from Genetic Perspective: An updated Review

Babaie

Omraninava

Gorabi

et al. 2022

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Psoriasis is an organ-specific autoimmune disease characterized by the aberrant proliferation and differentiation of keratinocytes, leading to skin lesions. Abnormal immune responses mediated by T cells and dendritic cells and increased production of inflammatory cytokines have been suggested as underlying mechanisms in the pathogenesis of psoriasis. Emerging evidence suggests that there is a heritable basis for psoriatic disorders. Moreover, numerous gene variations have been associated with the disease risk, particularly those in innate and adaptive immune responses and antigen presentation pathway. Herein, this article discusses the genetic implications of psoriatic diseases' etiopathogenesis to develop novel investigative and management options.

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Non-Invasive Assessment of Skin Surface Proteins of Psoriasis Vulgaris Patients in Response to Biological Therapy

Orro,

Salk,

Merkulova

et al. 2023

IJMS

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Measurements of skin surface biomarkers have enormous value for the detailed assessment of skin conditions, both for clinical application and in skin care. The main goals of the current study were to assess whether expression patterns of skin surface hBD-1, hBD-2, IL-1α, CXCL-1, and CXCL-8, examples of proteins known to be involved in psoriasis pathology, are associated with disease severity and whether expression patterns of these proteins on the skin surface can be used to measure pharmacodynamic effects of biological therapy. In this observational study using transdermal analysis patch (TAP), levels of skin surface IL-1α, hBD-1, hBD-2, CXCL-1/2, and CXCL-8 of psoriasis vulgaris (PV) patients over biological therapy were assessed. The Psoriasis Area Severity Index (PASI) and local score for erythema, induration, and desquamation were determined from the exact same skin area as FibroTx TAP measurements. Thirty-seven adult PV patients were included, of which twenty-three were subjected to anti-TNF-α, seven to anti-IL-17A, and seven to anti-IL12/IL-23 therapy. Significantly higher levels of hBD-1, hBD-2, CXCL-1/2, and CXCL-8 were detected on lesional skin compared to the non-lesional skin of the PV patients. In contrast, lower levels of IL-1α were found in lesional skin compared to non-lesional skin. In addition, we observed that the biomarker expression levels correlate with disease severity. Further, we confirmed that changes in the expression levels of skin surface biomarkers during biological therapy correlate with treatment response. Biomarker expression patterns in response to treatment differed somewhat between treatment subtypes. We observed that, in the case of anti-TNF-α therapy, an increase after a steady decrease in the expression levels of CXCL-1/2 and CXCL-8 occurred before the change in clinical scores. Moreover, response kinetics of skin surface proteins differs between the applied therapies—hBD2 expression responds quickly to anti-IL-17A therapy, CXCL-1/2 to anti-IL-12/23, and levels of CXCL-8 are rapidly down-regulated by IL-17A and IL-12/23 therapy. Our findings confirm that the skin surface hBD-2, IL-1α, CXCL-1/2, and CXCL-8 are markers for the psoriasis severity. Further, data obtained during this study give the basis for the conclusion that skin surface proteins CXCL-1/2 and CXCL-8 may have value as therapeutic biomarkers, thus confirming that measuring the ‘molecular root’ of inflammation appears to have value in scoring disease severity on its own.

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Lack of association between CARD10/CARMA3 tag SNPs and psoriasis vulgaris in the southern Chinese population

Cited by 3 publications

References 19 publications

Psoriasis: An Immunogenetic Perspective

Psoriasis: An Immunogenetic Perspective

Etiopathogenesis of Psoriasis from Genetic Perspective: An updated Review

Non-Invasive Assessment of Skin Surface Proteins of Psoriasis Vulgaris Patients in Response to Biological Therapy

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