Association of the TNF −238 promoter polymorphism with susceptibility to tuberculosis and malaria in Africa

Avs., Hill; Ruwende, Cyril; McGuire, William; Bellamy, Richard; Coleman, Emma; Ali, Sayed; Loke, Hsin; Corrah, Tumena; Snow, Robert W.; Marsh, K; Greenwood, Brian; Kjwp., McAdam; Whittle, H.C.; Kwiatkowski, D

doi:10.1016/0198-8859(96)85337-7

Cited by 5 publications

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“…The TNF238.2 variant has been shown to be in linkage disequilibrium with B18, B57, DR7, DR17.2, and to be part of the extended haplotypes B18-BFF1-DR17.2 (DRB1*0301) and B57-C4 A6-DR7-DQw9 [7,9]. The previously published data on HLA class I and DRB1* antigens in our population [13] were used to test TNF-a polymorphisms at positions ¹238 and ¹308 for linkage disequilibrium to HLA-B and HLA-DRB1 ( Table 2). Nine of 18 (50%) TNF238.2 alleles were observed in B57-positive patients (P < 0·00001; P corr < 0·001).…”

Section: Resultssupporting

confidence: 68%

“…Our data suggest that TNF238.2 and DRB1*1301-02 are independent factors encoded within the MHC that influence the outcome of acute hepatitis B infection. Disease susceptibility for infectious diseases is determined at such different functional levels as cytokine production and antigen presentation, as has been shown for malaria [11,13,31].…”

Section: Discussionmentioning

confidence: 99%

“…At position ¹308 TNF308.2 (A at ¹308) is associated with higher constitutive and inducible levels of TNF-a [9], whereas for the TNF238.2 allele (A at ¹238) functional consequences are not yet clear [10]. The TNF308.2 allele has been linked with susceptibility to cerebral malaria [11] and mucocutaneous leishmaniasis [12], whereas both TNF308.2 and TNF238.2 have been associated with tuberculosis and malarial anaemia [13].…”

Section: Introductionmentioning

confidence: 99%

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A tumour necrosis factor-alpha (TNF-α) promoter polymorphism is associated with chronic hepatitis B infection

HÖhler¹,

Krüger

Gerken³

et al. 1998

Clinical and Experimental Immunology

196

125

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Cytokines such as TNF-alpha and interferon gamma (IFN-gamma) are important for the elimination of infected hepatocytes during acute hepatitis B virus (HBV) infection. Two G versus A transitions in the TNF-alpha promoter region at positions -308 and -238 possibly influence TNF-alpha expression. We investigated these TNF-alpha polymorphisms in 71 patients with chronic HBV infection, in 32 subjects that had spontaneously recovered from acute HBV infection, and in 99 healthy controls. The -238 A promoter variant was present in 18 (25%) of 71 patients with chronic HBV infection compared with two (6%) of 32 subjects with acute infection (P<0.04), and seven (7%) of 99 controls (P<0.003). By contrast, the prevalence of the variant at position -308 was similar in all investigated groups. The observed differences could not be explained by linkage disequilibrium to HLA-B or -DRB1* alleles. These findings suggest an association between the TNF-alpha promoter polymorphism at position -238 and the development of chronic HBV infection. This promoter variant appears to be linked to defective viral clearance.

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Section: Resultssupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

A tumour necrosis factor-alpha (TNF-α) promoter polymorphism is associated with chronic hepatitis B infection

HÖhler¹,

Krüger

Gerken³

et al. 1998

Clinical and Experimental Immunology

196

125

View full text Add to dashboard Cite

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“…At position -308 allele 2 (A; TNF308.2) is associated with higher consti-tutive and inducible levels of TNF-␣ [Wilson et al, 1994] whereas for the TNF238.2 (A) allele at -238 functional consequences are not yet clear [Pociot et al, 1995]. The TNF308.2 allele has been linked with susceptibility to cerebral malaria [McGuire et al, 1994], mucocutaneous leishmaniasis [Cabrera et al, 1995], whereas both TNF308.2 and TNF238.2 have been associated with tuberculosis and malarial anaemia [Hill et al, 1996].…”

Section: Introductionmentioning

confidence: 99%

Tumor necrosis factor alpha promoter polymorphism at position -238 is associated with chronic active hepatitis C infection

et al. 1998

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Tumor necrosis factor alpha (TNF-alpha) is involved in the pathogenesis of chronic hepatitis C virus infection. The gene for TNF-alpha is encoded in the major histocompatibility locus (MHC). Two polymorphisms at positions -308 and -238 in the TNF-alpha promoter region might influence TNF-alpha expression. These promoter polymorphisms have been linked previously to a number of infectious diseases. TNF-alpha promoter polymorphisms at positions -238 and -308 were studied by DNA sequencing and sequence-specific oligonucleotide hybridization in 82 individuals with chronic hepatitis C and 99 control subjects. Subjects had been HLA class I and class II typed in a previous study. The frequency of the TNF238.2 promoter allele was significantly higher in the hepatitis C group (18.7%) compared to the controls (3.5%; P< 0.0001; pcorr < 0.009). No significant differences in the frequency of the TNF308.2 allele were observed between patients and controls. The increased frequency of the TNF238.2 allele could not be explained by linkage disequilibrium to HLA-B or -DR genes. These findings show an association between the TNF238.2 promoter variant and chronic active hepatitis C. They suggest that this polymorphism or a linked gene may be a host factor contributing to the development of chronic active hepatitis C.

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“…The SNP at position -238 has been associated with reduced TNF-α transcription (17,19) . The presence of the mutant -238A allele in patients with rheumatoid arthritis (13) , dengue with HIV (20) , or cancer (21) has been related to protection against and susceptibility to some diseases, such as chronic hepatitis B and C (22) , multiple sclerosis (23) and psoriasis in males (24) .…”

Section: Introductionmentioning

confidence: 99%

Distribuição de Polimorfismos de Base única (SNPs) no gene de TNF-alfa (-238/-308) entre pacientes com TB e outras pneumopatias: marcadores genéticos de susceptibilidade a ocorrência de TB?

Oliveira¹,

Silva²,

Costa³

et al. 2004

J. bras. pneumol.

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INTRODUÇÃO: Fatores genéticos podem desempenhar um importante papel na susceptibilidade à tuberculose (TB) ativa, e polimorfismos de base única (SNPs) em diferentes genes que codificam para citocinas têm sido descritos e associados com doenças. OBJETIVOS: Investigar o quanto polimorfismo na região promotora do gene que codifica para TNF-alfa (-238 e -308) estão associados a ocorrência de TB ativa. MÉTODOS: SNPs dentro do gene de TNF-alfa foram analisados por PCR- RFLP em dois grupos de indivíduos: pacientes com TB (n = 234) e pacientes com pneumopatias não TB (n = 113). RESULTADOS: Neste estudo, o alelo -238A esteve associado significantemente com susceptibilidade à ocorrência de TB e gravidade das formas clínicas (p = 0,00002; OR = 0,15; IC = 0,06-0,36). Por outro lado, o alelo -308A esteve associado significantemente com a proteção a outras formas de doença pulmonar (p = 0,02; OR = 1,95; IC = 1,07-3,58). CONCLUSÕES: Estes resultados preliminares sugerem a importância de estudos genéticos na ocorrência da TB. São necessários outros estudos para melhorar a compreensão sobre a patogênese do M. tb.

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Association of the TNF −238 promoter polymorphism with susceptibility to tuberculosis and malaria in Africa

Cited by 5 publications

References 0 publications

A tumour necrosis factor-alpha (TNF-α) promoter polymorphism is associated with chronic hepatitis B infection

A tumour necrosis factor-alpha (TNF-α) promoter polymorphism is associated with chronic hepatitis B infection

Tumor necrosis factor alpha promoter polymorphism at position -238 is associated with chronic active hepatitis C infection

Distribuição de Polimorfismos de Base única (SNPs) no gene de TNF-alfa (-238/-308) entre pacientes com TB e outras pneumopatias: marcadores genéticos de susceptibilidade a ocorrência de TB?

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