IL-23R gene polymorphisms in rheumatoid arthritis

Soysal, Ergün; Ulutaş, Firdevs; Tepeli, Emre; Kaymaz, Serdar; Çobankara, Veli

doi:10.1007/s00296-021-04881-9

Cited by 8 publications

(7 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Statistical analysis was performed by IBM SPSS Statistics 25.0 (IBM Co., Armonk, NY, USA) and p -values <0.01 were considered significant. 41…”

Section: Discussionmentioning

confidence: 99%

Bone marrow mesenchymal stem cells response on collagen/hyaluronan/chondroitin scaffold enriched with gentamicin -loaded gelatin microparticles for skin tissue engineering

Wang

et al. 2023

J Biomater Appl

View full text Add to dashboard Cite

The repair and functional reconstruction of large skin defects caused by burn remains an intractable clinical problem. Collagen type I (ColI) was extracted from carp scales and confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis ultraviolet adsorption spectra and automatic amino acid analyzer. Then the scaffolds containing the purified ColI, hyaluronic acid (HA) and chondroitin sulfate (CS) were constructed and examined. The results showed that the scaffold (ColI:CS:HA=9:1:1) had larger pore diameter, porosity, water absorption, degradation rate and tensile strength. gentamycin sulphate (GS) - gelatin microspheres (GMSs) were prepared by emulsion cross-linking method. The drug release study of the ColI-CS-HA-GS/GMSs scaffold with antibacterial property showed a prolonged, continuous, and sustained release of GS. The bone marrow mesenchymal stem cells (BMSCs) were extracted from rat and inoculated into the ColI-HA-CS-GS/GMSs scaffold. The results performed that the scaffold could accelerate proliferation of the BMSCs and wound healing.

show abstract

“…Statistical analysis was performed by IBM SPSS Statistics 25.0 (IBM Co., Armonk, NY, USA) and p -values <0.01 were considered significant. 41…”

Section: Discussionmentioning

confidence: 99%

Bone marrow mesenchymal stem cells response on collagen/hyaluronan/chondroitin scaffold enriched with gentamicin -loaded gelatin microparticles for skin tissue engineering

Wang

et al. 2023

J Biomater Appl

View full text Add to dashboard Cite

show abstract

“…Rheumatoid arthritis risk may rise due to the increased production of IL-23R that is linked to particular SNP alleles in its gene. A putative mechanism for the onset of rheumatoid arthritis, the IL-23/Th17 signaling pathway, which contains genes that generate IL-23/IL-23R, IL-17A, and IL-17F, may also play a role in disease susceptibility and progression [46]. Altamemi et al (2017) investigated the relationship between RA in Iraqi patients and the rs11209026 SNP in the IL-23R gene.…”

Section: Il-23r Gene Polymorphismmentioning

confidence: 99%

The Association of Genetic Polymorphisms in Tumor Necrosis Factor-Alpha and Interleukins with Disease Severity or Response to Biological Therapy in Iraqi Rheumatoid Arthritis Patients: A Narrative Review

Mohammed¹,

Jamal²,

Alshamari³

2023

Al-Rafidain J Med Sci

View full text Add to dashboard Cite

Background: Tumor necrosis factor-alpha (TNF-α) and interleukins play important roles in the pathogenesis of rheumatoid arthritis (RA). Genetic research has been employed to find many of the missing connections between genetic risk variations and causal genetic components. Objective: The goal of this study is to look at the genetic variations of TNF-α and interleukins in Iraqi RA patients and see how they relate to disease severity or response to biological therapy. Method: Using specific keywords, the authors conducted a systematic and comprehensive search to identify relevant Iraqi studies examining the genetic variations of TNF-α and interleukins in Iraqi RA patients and how they relate to disease severity or response to biological therapy. Results: Thirteen studies have looked at TNF-α and interleukin genetic polymorphisms in Iraqi RA patients. Only the IL-2, IL-4, IL-6, IL-17, and IL-23 receptor gene polymorphisms were explored for interleukins; however, the results of studies indicate no association between genetic polymorphism and the severity of RA. Very few researchers examine the correlation between genetic variation and TNF-α inhibitor responsiveness. Numerous studies have been conducted to investigate the genetic variations of the TNF-α promoter. The -308 G/A region in the promotor region was the most studied location.

show abstract

“…Existen otros genes no antígeno del leucocito humano estudiados como la proteína tirosina fosfatasa no receptora tipo 22 (PTPN22) [5,6] representando en este grupo de moléculas la de mayor susceptibilidad para artritis reumatoide, la cual está relacionada con riesgo para otras enfermedades autoinmunes como diabetes mellitus tipo 1, artritis idiopática juvenil, lupus eritematoso sistémico, síndrome de Sjogren, enfermedad tiroidea autoinmune, vitíligo y diferentes formas de vasculitis. Igualmente se ha analizado polimorfismo del gen antígeno-4 de linfocitos T citotóxicos (CTLA-4) [7,8] y la desregulación del receptor de interleucina-23 (IL-23R) como predisposición para artritis reumatoide, y otras condiciones reumáticas como la espondilitis anquilosante y lupus eritematoso sistémico [9,10]. Sin embargo, no explican del todo los mecanismos fisiopatológicos de la enfermedad, debido a las características de patrón de herencia poligénica.…”

Section: Introductionunclassified

Effect of epigenetics on rheumatoid arthritis

Rada¹,

Mestre²,

Morales³

2023

Medwave

View full text Add to dashboard Cite

Rheumatoid arthritis is an autoimmune and inflammatory disease that predominantly affects the diarthrodial joints. In this pathology, environmental or behavioral factors can act in synergy with genetic predisposition, accelerating the onset and severity of the disease. This link between the environment and the genome is mediated by epigenetic marks on deoxyribonucleic acid, including its methylation, histone modification, and noncoding ribonucleic acid-mediated regulation. Epigenetics can generate heritable phenotypic changes, which are not determined by modifications in the deoxyribonucleic acid sequence and are therefore reversible. Therefore, diet, medications and other environmental factors would have the ability to modulate them. The identification of a specific epigenetic dysregulation can offer a better understanding of the pathophysiology of the disease and positively influence the prevention, diagnosis and development of new therapeutic targets. Rheumatoid arthritis is an autoimmune and inflammatory disease that predominantly affects the diarthrodial joints. In this pathology, environmental or behavioral factors can act in synergy with genetic predisposition, accelerating the onset and severity of the disease. This link between the environment and the genome is mediated by epigenetic marks on deoxyribonucleic acid, including its methylation, histone modification, and noncoding ribonucleic acid-mediated regulation. Epigenetics can generate heritable phenotypic changes, which are not determined by modifications in the deoxyribonucleic acid sequence and are therefore reversible. Therefore, diet, medications and other environmental factors would have the ability to modulate them. The identification of a specific epigenetic dysregulation can offer a better understanding of the pathophysiology of the disease and positively influence the prevention, diagnosis and development of new therapeutic targets.

show abstract

IL-23R gene polymorphisms in rheumatoid arthritis

Cited by 8 publications

References 25 publications

Bone marrow mesenchymal stem cells response on collagen/hyaluronan/chondroitin scaffold enriched with gentamicin -loaded gelatin microparticles for skin tissue engineering

Bone marrow mesenchymal stem cells response on collagen/hyaluronan/chondroitin scaffold enriched with gentamicin -loaded gelatin microparticles for skin tissue engineering

The Association of Genetic Polymorphisms in Tumor Necrosis Factor-Alpha and Interleukins with Disease Severity or Response to Biological Therapy in Iraqi Rheumatoid Arthritis Patients: A Narrative Review

Effect of epigenetics on rheumatoid arthritis

Contact Info

Product

Resources

About