Evidence map›Paper›PMID 31090825›Full record

ArticleAnais brasileiros de dermatologia

The role of GNLY gene polymorphisms in psoriasis pathogenesis.

Esra Ermis, Sevim Karakas Celik, Nilgun Solak, Gunes Cakmak Genc, Ahmet Dursun

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Article in Anais brasileiros de dermatologia. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Evaluation of the relationship ofPostepy dermatologii i alergologii · 2021
    Article
  8. Review
  9. Role of Innate Immune Cells in Psoriasis.International journal of molecular sciences · 2020
    Review
  10. Article
4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Esra ErmisDepartment of Molecular Biology and Genetics, Faculty of Sciences and Arts, Bulent Ecevit University, Zonguldak, Turkey.ORCID 0000-0001-6233-2420
Sevim Karakas CelikDepartment of Molecular Biology and Genetics, Faculty of Sciences and Arts, Bulent Ecevit University, Zonguldak, Turkey.ORCID 0000-0003-0505-7850
Nilgun SolakDepartment of Dermatology, Faculty of Medicine, Bulent Ecevit University, Zonguldak, Turkey.ORCID 0000-0002-6572-9615
Gunes Cakmak GencDepartment of Medical Genetics, Faculty of Medicine, Bulent Ecevit University, Zonguldak, Turkey.ORCID 0000-0001-7222-0377
Ahmet DursunDepartment of Medical Genetics, Faculty of Medicine, Bulent Ecevit University, Zonguldak, Turkey.ORCID 0000-0002-7625-837X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPsoriasis is a systemic inflammatory disorder that involves complex pathogenic interactions between the innate and adaptive immune systems. The most accepted mechanism in the etiopathogenesis of psoriasis is the induction of inflammation with keratinocyte hyperproliferation. Granulysin (GNLY) is a cytolytic antimicrobial peptide (AMP) that is secreted together with granzyme and perforin from the granules of human cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. It has been immunohistochemically proven that the expression of granulysin is increased in lesions of psoriasis.

objectiveThis study aimed to investigate the relationship between psoriasis disease and granulysin gene polymorphisms.

methodsGNLY rs7908 and rs10180391 polymorphisms were studied by PCR-RFLP in 100 psoriasis patients under treatment in the Dermatology Polyclinic of Bulent Ecevit University. In addition, 100 healthy individuals with similar age and sex distribution were used as a control group.

resultsIn the control group, GNLY rs7908 CC genotype was significantly higher than in psoriasis patients (P= 0.031; OR= 0.305; Cl= 0.305 (0.121 - 0.773). In our study, the genotype distributions in patients and control groups were GNLY rs7908 (SNP) GG (51%, 37%), GC (41%, 44%), CC (8%, 19%); GNLY rs10180391 (SNP) from the CC (41%, 44%), CT (42%, % 41), TT (17%, 15%). STUDY LIMITATIONS: The study only included Turkish patients.

conclusionOur findings showed that GNLY rs7908 CC genotype and C allele had a protective effect against psoriasis and decreased the disease severity (according to PASI score), whereas rs10180391 SNP did not show any effective role in psoriasis pathogenesis.

Indexed as

AdultAllelesAntigens, Differentiation, T-LymphocyteCase-Control StudiesFemaleGene ExpressionGenotypeHumansMaleMiddle AgedPolymorphism, GeneticProtective AgentsPsoriasisSeverity of Illness IndexAntigens, Differentiation, T-LymphocyteGNLY protein, humanProtective Agents

Identifiers

PMID31090825
PMCPMC6486070

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.