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Autoimmunity and tuberculosis. Opposite association with TNF polymorphism.

dc.creatorAnaya, Juan-Manuel
dc.creatorCorrea, Paula A.spa
dc.creatorGomez, Luis M.spa
dc.creatorCadena, Josespa
dc.date.accessioned2020-08-19T14:41:33Z
dc.date.available2020-08-19T14:41:33Z
dc.date.created2005-02spa
dc.description.abstractObjective. To examine the influence of the –308 and –238 single nucleotide polymorphisms (SNP) of tumor necrosis factor-? gene (TNF) on patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), primary Sjögren’s syndrome (SS), and tuberculosis (TB). Methods. Genomic DNA from patients with RA (n = 165), SLE (n = 100), primary SS (n = 67), and TB (n = 135) and ethnically matched controls (n = 430) was genotyped for TNF –308 and –238 SNP by PCR-RFLP. Results. TNF –308A allele was associated with RA (odds ratio, OR 1.8, p = 0.002), SLE (OR 2.6, p < 0.0001), and primary SS (OR 2.9, p < 0.0001). TNF –308G was associated with TB (OR 1.8, p = 0.02). The –308 GG genotype was protective for autoimmunity (p < 0.003). TNF –238A allele was protective for autoimmunity but represented a susceptibility factor for TB (OR 2.2, p < 0.0001). Haplotype –308A–238G was a protective factor against TB, whereas it carried susceptibility for RA, SLE, and primary SS (p < 0.0001). Conclusion. The results show an opposite association of TNF polymorphism with autoimmunity and TB, and suggest the existence of heterozygote advantage, sustaining the hypothesis that autoimmune diseases are a consequence of natural selection for enhanced TB resistance. Data also provide genetic evidence supporting the common variants/multiple disease hypothesis, which emphasizes that many disease genes may not be disease-specific, and that similar immunogenetic mechanisms underlie autoimmune diseases.eng
dc.format.mimetypeapplication/pdf
dc.identifier.issnISSN: 0120-4157
dc.identifier.issnEISSN: 2590-7379
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/27270
dc.language.isoengspa
dc.publisherInstituto Nacional de Saludspa
dc.relation.citationEndPage224
dc.relation.citationIssueNo. 2
dc.relation.citationStartPage219
dc.relation.citationTitleBiomedica. Revista del Instituto Nacional de Salud
dc.relation.citationVolumeVol. 32
dc.relation.ispartofBiomedica. Revista del Instituto Nacional de Salud, ISSN: 0120-4157 ; EISSN: 2590-7379, Vol.32, No.2 (2005); pp. 219-224 spa
dc.relation.urihttps://www.jrheum.org/content/jrheum/32/2/219.full.pdfspa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.sourceBiomedica. Revista del Instituto Nacional de Saludspa
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR
dc.subject.keywordTumor Necrosis Factorspa
dc.subject.keywordRheumatoid Arthritisspa
dc.subject.keywordTuberculosisspa
dc.subject.keywordSystemic Lupus Erythematosusspa
dc.subject.keywordSjögren’s Syndromespa
dc.subject.keywordAutoimmunityspa
dc.titleAutoimmunity and tuberculosis. Opposite association with TNF polymorphism.spa
dc.title.TranslatedTitleAutoinmunidad y tuberculosis. Asociación opuesta con polimorfismo de TNF.spa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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