ArticleClinical rheumatology2015
C-reactive protein gene and Toll-like receptor 4 gene polymorphisms can relate to the development of psoriatic arthritis.
Article in Clinical rheumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Targeting Toll-like Receptor (TLR) Pathways in Inflammatory Arthritis: Two Better Than One?Biomolecules · 2021Review
- Overview of the molecular determinants contributing to the expression of Psoriasis and Psoriatic Arthritis phenotypes.Journal of cellular and molecular medicine · 2020Review
- Epigenetics and innate immunity: the 'unTolld' story.Immunology and cell biology · 2016Review
- The critical role of toll-like receptors--From microbial recognition to autoimmunity: A comprehensive review.Autoimmunity reviews · 2016Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to determine in psoriatic arthritis (PsA) patients the Toll-like receptor (TLR) 4 and C-reactive gene (CRP) polymorphisms and allele frequency and to investigate the relationship between clinical parameters and gene polymorphisms. We enrolled in this study 31 PsA and 41 healthy control subjects. PsA diagnosis was according to CASPAR criteria. Bath ankylosing spondylitis diseases activity index, Maastricht ankylosing spondylitis enthesitis score, and Bath ankylosing spondylitis functional index were measured. C, A, and T alleles of CRP and A and G alleles of TLR 4 were determined using the analysis of melting curves after real-time PCR. CRP A, C, and T allele frequency in controls was 26.8, 73.2, and 36.6%, respectively. In the PsA patient group, A, C, and T allele frequency was 9.7, 87.1, and 12.9%, respectively. Between control and PsA groups, there was a significant difference in A, C, and T allele frequency (P = 0.008, 0.038, and 0.001, respectively). The frequency of CRP gene polymorphisms (CA, AA, CT, TA, and TT alleles) in the control group was 56.1% and in the PsA group was 22.6%. There was a significant difference between the two groups (P = 0.004). The absence of a CRP gene polymorphism was a risk factor for PsA (odds ratio 4.3, 95% CI; 1.5-12.4, P = 0.005). TLR gene haploid frequency was investigated, and all control subjects had the wild-type AA allele. PsA patient GA allele frequency was 6.5%. There was no significant difference between the two groups (P = 0.182). GA mutant allele frequency was related to PsA (odds ratio 7.03, 95% CI; 0.32-151.9, P = 0.214). We have shown that CRP gene polymorphisms are higher in control subjects than PsA patients, and TLR 4 gene polymorphisms were found to be related to PsA.
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