Previous findings regarding the role of TNF-alpha-308 gene polymorphism in multiple sclerosis (MS) are contradictory. The aim of this study was to investigate the possible influence of TNF-alpha-308 polymorphism on MS susceptibility and the MS disease process in a Croatian and Slovenian population. Genotyping was performed in 338 patients and 460 healthy controls. The TNF2 allele was present in 123 (26.8%) healthy controls vs. 67 (19.9%) MS patients (p = 0.023, odds ratio = 0.68, 95% confidence interval = 0.48-0.95), suggesting that carriage of the TNF2 allele might decrease MS risk. The difference in TNF2 allele carrier frequency between patients and controls was identified in the relapsing-remitting MS group. There was no association between TNF2 allele carrier status and age at disease onset or disease progression. Our results suggest that, in the study populations, the TNF-alpha-308 polymorphism may play a role in MS susceptibility.
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http://dx.doi.org/10.1159/000099159 | DOI Listing |
Int J Rheum Dis
May 2016
Hemostasis and Thrombosis Laboratory, Hospital of Infectious Diseases "F. J. Muñiz", Buenos Aires, Argentina.
Aim: A polymorphism in the tumor necrosis factor-alpha (TNF-α) promoter region has been associated with disease susceptibility and progression in rheumatoid arthritis (RA). The presence of an adenosine (TNF2 allele) instead of a guanine (TNF1 allele) at position -308 may be responsible for a general increase in the transcriptional activity of the TNF-α gene. Our aim was to evaluate the association of the TNF2 allele with the risk of disease development and/or progression of RA in an Argentine population cohort.
View Article and Find Full Text PDFPLoS One
February 2015
Departamento de Bioquimica y Medicina Molecular, Facultad de Medicina, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon, Mexico; Centro de Investigacion y Desarrollo en Ciencias de la Salud, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon, Mexico.
Unlabelled: Environmental and genetic factors may modify or contribute to the phenotypic differences observed in multigenic and monogenic diseases, such as cystic fibrosis (CF). An analysis of modifier genes can be helpful for estimating patient prognosis and directing preventive care. The aim of this study is to determine the association between seven genetic variants of four modifier genes and CF by comparing their corresponding allelic and genotypic frequencies in CF patients (n = 81) and control subjects (n = 104).
View Article and Find Full Text PDFPathog Glob Health
January 2013
Malaria Research Unit, Department of Parasitology, Faculty of Medicine, University of Colombo, Sri Lanka.
Plasma levels of pro- and anti-inflammatory cytokines of Plasmodium falciparum-infected patients with severe malaria (SM; n = 62) and uncomplicated malaria (UM; n = 69) from Sri Lanka were assessed. SM patients had significantly higher levels of TNF-alpha (P < 0·01), IL-6 (P < 0·01), and IL-10 (P < 0·05) compared to the UM patients. Plasma IL-2 levels of these patients were undetectable.
View Article and Find Full Text PDFCytokine
February 2013
Clínica de Artrite Reumatoide, Hospital Adriano Jorge, Manaus, Brazil.
Purpose: The aim of this study was to investigate the influence of the TNF -308 G/A polymorphism in the promoter region of the tumor necrosis factor-α gene on the susceptibility and severity of rheumatoid arthritis (RA) in individuals from the Brazilian Amazon.
Methods: A total of 323 individuals-192 healthy controls without arthritis and 131 individuals suffering from arthritis-were genotyped for this polymorphism using a methodology based on PCR-RFLP.
Results: The frequency of the A allele (TNF2) in rheumatoid arthritis sufferers was not significantly higher than in the controls (p=0.
Int J Dermatol
May 2012
Departamento de Dermatología, Hospital Universitario Dr José Eleuterio González, Monterrey, NL, México.
Background: Alopecia areata (AA) is a chronic inflammatory condition characterized by hair loss, most frequently from the scalp. Its etiopathogenesis is currently unknown, but inflammatory traits and associations with autoimmune diseases suggest that AA shares a similar origin. The tumor necrosis factor alpha (TNFα) gene, located on chromosome 6 within the major histocompatibility complex class III gene, may carry previously described polymorphisms--particularly in the promoter region, such as TNFα-308G/A--known to be risk factors in a wide variety of inflammatory pathologies.
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