scholarly journals TNF-αPolymorphisms in Juvenile Idiopathic Arthritis: Which Potential Clinical Implications?

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
A. Scardapane ◽  
L. Breda ◽  
M. Lucantoni ◽  
F. Chiarelli
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Large Scale ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Single Nucleotide ◽  
Adult Rheumatoid Arthritis ◽  
Functional Consequences ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Important Cytokine

Whether tumor necrosis factor alpha (TNF-α) gene polymorphisms (SNPs) influence disease susceptibility and treatment of patients with juvenile idiopathic arthritis (JIA) is presently uncertain. TNF-αis one of the most important cytokine involved in JIA pathogenesis. Several single nucleotide polymorphisms (SNPs) have been identified within the region of the TNF-αgene but only a very small minority have proven functional consequences and have been associated with susceptibility to JIA. An association between some TNF-αSNPs and adult rheumatoid arthritis (RA) susceptibility, severity and clinical response to anti-TNF-αtreatment has been reported. The most frenquetly studied TNF-αSNP is located at −308 position, where a substitution of the G allele with the rare A allele has been found. The presence of the allele −308A is associated to JIA and to a poor prognosis. Besides, the −308G genotype has been associated with a better response to anti-TNF-αtherapy in JIA patients, confirming adult data. Psoriatic and oligoarticular arthritis are significantly associated to the −238 SNP only in some works. Studies considering other SNPs are conflicting and inconclusive. Large scale studies are required to define the contribution of TNF-αgene products to disease pathogenesis and anti-TNF-αtherapeutic efficacy in JIA.

Tumor necrosis factor-alpha single nucleotide polymorphisms in juvenile systemic lupus erythematosus

2015 ◽  
Vol 76 (8) ◽  
pp. 533-536 ◽  
Author(s):  
Fatemeh Tahghighi ◽  
Vahid Ziaee ◽  
Mohammad Hassan Moradinejad ◽  
Arezou Rezaei ◽  
Sara Harsini ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Nucleotide Polymorphisms ◽  
Systemic Lupus ◽  
Juvenile Systemic Lupus Erythematosus ◽  
Necrosis Factor Alpha ◽  
Single Nucleotide ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Evaluation of polymorphisms in inflammatory mediator and cellular adhesion genes as risk factors for feline infectious peritonitis

2019 ◽  
Vol 22 (6) ◽  
pp. 564-570 ◽  
Author(s):  
Helen Kedward-Dixon ◽  
Emi N Barker ◽  
Séverine Tasker ◽  
Anja Kipar ◽  
Christopher R Helps
Keyword(s):  
Inflammatory Mediator ◽  
Cellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Single Nucleotide ◽  
Feline Infectious Peritonitis ◽  
Genes Encoding ◽  
Factor Alpha ◽  
Necrosis Factor

Objectives Feline infectious peritonitis (FIP) is a high mortality infectious disease. Single nucleotide polymorphisms (SNPs) in the genes encoding interferon gamma ( IFNG), tumour necrosis factor alpha ( TNFA) and dendritic cell-specific intercellular adhesion molecule-grabbing non-integrin (DC-SIGN; CD209) have been associated with increased and decreased risk of developing FIP. This study was designed to determine whether these associations were present in a UK population of pedigree cats using samples from cats euthanased with a confirmed diagnosis (FIP, n = 22; non-FIP, n = 10) or clinically healthy cats over 11 years of age (n = 3). Methods DNA was extracted from tissue (n = 32) or blood (n = 3) and PCR performed for regions of IFNG, TNFA and CD209. PCR amplicons were sequenced, each SNP genotype was determined, and genotype/allele frequency for each SNP and FIP status were compared. Results No significant association was found between the genotype and FIP status for any SNP analysed. There was a trend for the heterozygous CT genotype at both IFNG g.401 and IFNG g.408 to be associated with FIP ( P = 0.13), but this genotype was also found in a substantial proportion of non-FIP cats. There was also a trend for the heterozygous CT genotype at IFNG g.428 to be associated with FIP ( P = 0.06), although most cats with FIP had the CC genotype at this locus. No associations were found between any allele at TNFA g.-421, CD209 g.1900, CD209 g.2276, CD209 g.2392 and CD209 g.2713 and FIP. Conclusions and relevance The use of the IFNG, TNFA and CD209 SNPs described to predict the risk of FIP cannot currently be recommended.

scholarly journals Tumor Necrosis Factor Alpha-863 C/A Single Nucleotide Polymorphisms and Nephrotic Syndrome

2020 ◽  
Vol 10 (03) ◽  
pp. 319-322
Author(s):  
Ahmed Abdul-Hassan Abbas ◽  
Zainab J. Fadhil ◽  
Shatha Hussein Ali
Keyword(s):  
Nephrotic Syndrome ◽  
Tumor Necrosis Factor ◽  
Serum Level ◽  
Tumor Necrosis ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Single Nucleotide ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Introduction: Cytokines act as a mediator of inflammation in childhood nephrotic syndrome. Polymorphisms of cytokines genes may influence susceptibility to nephrotic syndrome (NS), as well as, patients’ steroid responses. Objective: To study the association of tumor necrosis factor-alpha single nucleotide polymorphisms (TNF-α SNP) (-863 C/A) with the development of NS in addition to access to their effects on serum level of TNF and the response to steroid therapy. Patients and Methods: This study included 60 patients (19 female and 41 male) with nephrotic syndrome; their ages ranged from 2 to 18 years. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to assess the TNF-α gene polymorphism. Results: According to the digestion pattern of RFLP-PCR products of TNF-α-863, this polymorphism had three genotypes, which were CC, CA, and AA, in both NS patients and controls. Also, the current result observed that -863 SNP do not affect the serum level of TNF-α and steroid responsiveness in patients with nephrotic syndrome. Conclusion: This polymorphism did not show any significant association with response to steroid therapy and TNF serum level neither at genotype nor at allele level.

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