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POLYMORPHISM OF THE HUMAN TNF PROMOTER REGION IN BRAZILIAN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS.
Author(s) -
Pancoto João Alexandre Trés,
Mendes Junior Celso T.,
LucisanoValim Yara M.,
DiasBaruffi Marcelo,
Donadi Eduardo A.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.664.9
Subject(s) - immunology , pathogenesis , genotype , allele , autoantibody , proinflammatory cytokine , tumor necrosis factor alpha , autoimmunity , autoimmune disease , lupus erythematosus , medicine , cytokine , biology , genetics , gene , antibody , inflammation
Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by multisystemic organ involvement, polyclonal B‐cell activation and the production of autoantibodies. Several family studies have shown convincing evidences of multiple genetic loci associated with SLE development. TNF is a potent proinflammatory cytokine that plays an important role in the pathogenesis of SLE, and certain alleles of the tumor necrosis factor (TNF) gene have been consistently associated with the disease, particularly the ‐308‐A/G functional promoter polymorphism. In the present study we analyzed the allelic distribution of TNF‐308A/G in Brazilian SLE patients. METHODS AND RESULTS: A total of 148 SLE patients and 130 matched healthy controls were typed for the TNF‐308A/G polymorphism by polymerase chain reaction using allele‐specific oligonucleotide primers. A significant increase of the TNF G/A 308 genotype was observed in SLE patients when compared with healthy controls (p < 0.0001; OR = 7.156; 95% I. C.: 3.462–14.792). CONCLUSIONS: Since the Brazilian population is highly genetically diverse, the results reported here are in agreement with those reported for other populations, and corroborate the role of TNF in disease pathogenesis and the TNF‐308A/G genotype, which has been associated with high production of TNF, as conferring susceptibility to the disease. RESEARCH SUPPORT: CAPES