Scarring trachoma is associated with polymorphism in the tumor necrosis factor alpha (TNF-alpha) gene promoter and with elevated TNF-alpha levels in tear fluid

Conway, David J.; Holland, Martin J.; Bailey, Robin L.; Campbell, Alison E.; Mahdi, Olaimatu S.; Jennings, Richard T.; Mbena, E.; Mabey, David

doi:10.1128/iai.65.3.1003-1006.1997

Cited by 185 publications

(64 citation statements)

References 36 publications

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“…In our study, the frequency of the TNF2 allele reached only 11.7%, which is in agreement with previous studies performed in different Argentine subpopulations [32][33][34] and it is also similar to what had been reported in studies in Chilean, French and Chinese populations. However, it is very different from Caucasian and other Asian populations where the presence of the allele reached frequencies of up to 23% [35][36][37][38][39][40][41][42][43][44][45][46] (Table 3). In particular, the Argentinean population is the result of genetic admixture processes involving three continental contributors: Native Americans, western Africans and Europeans (mainly Spaniards and Italians), although the African component detected in different studies was very low (< 4%).…”

Section: Discussionmentioning

confidence: 75%

The −308 G/A polymorphism in the tumor necrosis factor-α gene is not associated with development and progression of rheumatoid arthritis in Argentinean patients

et al. 2014

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Section: Discussionmentioning

confidence: 75%

The −308 G/A polymorphism in the tumor necrosis factor-α gene is not associated with development and progression of rheumatoid arthritis in Argentinean patients

et al. 2014

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“…As it has been documented in other situations, it may reflect either a primary phenomenon [26] or a secondary phenomenon linked to the intensity of the inflammation [27]. An increased TNF2 frequency has been described in several infectious diseases associated with high production of TNF-a [28,29]. Moreover, TNF2 allele has been associated with increased TNF-a transcription [19] and also production by isolated peripheral blood mononuclear cells [20] as well as in a whole blood cell culture model [21], although these associations were not always found [30,31].…”

Section: Discussionmentioning

confidence: 92%

Tumour necrosis factor (TNF) gene polymorphism in Crohn’s disease (CD): influence on disease behaviour?

Louis

Peeters

Franchimont

et al. 2000

Clinical and Experimental Immunology

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SUMMARYCrohn's disease (CD) is a multifactorial disease with genetic heterogeneity. TNF-a plays a key role in the development of the mucosal lesions. The aim of our work was to study a single base pair polymorphism located in the promoter region of TNF gene, in a large population of CD patients with well defined phenotypes. One hundred and ninety-three patients with CD and 98 ethnically matched controls were studied. The ¹308 single base pair polymorphism of TNF gene was studied using an allele-specific polymerase chain reaction. Genotype and allelic frequencies were compared between patients and controls and between subgroups of patients defined by sex, age at diagnosis, familial history, location of disease, type of disease, extra-intestinal manifestations, and response to steroid treatment. In 29 patients a measure of TNF-a production by colonic biopsies was performed. The frequency of the allele TNF2 as well as the proportion of carriers of the allele TNF2 were slightly but not significantly lower in CD than in controls (11·9% versus 14·8% and 21·5% versus 27·6%, respectively). A more prominent difference in frequencies of allele TNF2 and in proportions of TNF2 carriers was found when comparing subgroups of patients. The frequency of allele TNF2 was significantly higher in steroid-dependent than in non-steroid-dependent disease (28·1% versus 10·3%; D ¼ 17·8%, 95% confidence interval (CI) ¼ 6·3-29·5%, P ¼ 0·0027) and tended to be higher in colonic than in small bowel disease and in fistulizing than in stricturing disease. Furthermore, TNF2 carriers tended to be more frequent in patients with steroid-dependent than non-steroid-dependent disease (43·8% versus 19·3%; D ¼ 24·5%, 95% CI ¼ 3·6-45·4%, P ¼ 0·022), in patients with fistulizing than stricturing disease (26·5% versus 9·6%; D ¼ 16·9%, 95% CI ¼ 1·1-32·6%, P ¼ 0·036), and in patients with colonic than small bowel disease (26·5% versus 11·1%; D ¼ 15·4%, 95% CI ¼ ¹0·8-31·6%, P ¼ 0·063). Finally, patients carrying at least one copy of allele 2 were found to produce slightly more TNF-a at the colonic level. The ¹308 TNF gene polymorphism may have a slight influence on the behaviour of CD. The carriage of allele 2 may favour steroid-dependent disease and to a lesser extent fistulizing and colonic disease, possibly secondary to a more intense TNF-a-driven inflammatory reaction at the mucosal level.

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“…However, other reporter gene studies have not been able to reproduce the effect of this polymorphism on up-regulation of TNF-a production [14,15]. In addition, Conway et al [16] found that scarring trachoma was also associated both with TNFA-308.2 polymorphism and with elevated TNF-a levels in tear fluid; however, detection of TNF-a in tear fluid samples was not associated with particular TNFA promoter genotypes.…”

Section: Discussionmentioning

confidence: 99%

TNFA promoter polymorphism and susceptibility to brucellosis

Caballero

Bravo

Nieto

et al. 2000

Clinical and Experimental Immunology

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SUMMARYThe aim of this study was to investigate the possible influence of the tumor necrosis factor alpha (TNFA) gene promoter polymorphisms and HLA class II genes on the susceptibility to or development of human brucellosis. TNFA genotypes (at positions 2308 and 2238) were determined in 59 patients with brucellosis and 160 healthy controls by polymerase chain reaction-restriction fragment length polymorphism. There were no significant differences between the patients and the controls for the TNFA-238 genotypes. However, when the overall TNFA-308 genotype distribution of the brucella patients was compared with that of the control subjects, a significant skewing was observed (P 0´02). The TNFA-308.1/2 genotype was present at significantly higher frequency in the total patient as a whole compared with control subjects (30% versus 15%; P 0´01, odds ratio (OR) 2´49, 95% confidence interval (CI) 1´16±5´33). No statistically significant differences in the distribution of HLA-DRB1 or DQB1 alleles were observed between brucella patients and control subjects. Stratification to correct for interdependence of TNFA-308.2 and HLA-DR3 alleles confirmed that, in spite of their strong linkage disequilibrium, the association of TNFA-308.2 with brucellosis was independent of HLA-DR3.

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Scarring trachoma is associated with polymorphism in the tumor necrosis factor alpha (TNF-alpha) gene promoter and with elevated TNF-alpha levels in tear fluid

Cited by 185 publications

References 36 publications

The −308 G/A polymorphism in the tumor necrosis factor-α gene is not associated with development and progression of rheumatoid arthritis in Argentinean patients

The −308 G/A polymorphism in the tumor necrosis factor-α gene is not associated with development and progression of rheumatoid arthritis in Argentinean patients

Tumour necrosis factor (TNF) gene polymorphism in Crohn’s disease (CD): influence on disease behaviour?

TNFA promoter polymorphism and susceptibility to brucellosis

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