Abstract
We have described suggestive linkage between microsatellite markers within the cytogenetic region 18q21–23 and SLE, a region where linkage with other autoimmune diseases has also been detected. The Bcl-2 gene located within this region, is a candidate gene because of its role in apoptosis, a physiological mechanism that could be deregulated in autoimmune disease. Furthermore, several studies have found abnormalities of Bcl-2 expression in SLE patients. We therefore sought to determine if the Bcl-2 gene is involved in SLE by studying members of a large cohort of Mexican SLE patients (n = 378) and 112 Swedish simplex families. Using a microsatellite marker and two single nucleotide polymorphisms located within the gene, we were unable to detect association between Bcl-2 and SLE in either population. We also tested whether combinations of alleles of the Bcl-2 and IL-10.G microsatellites would increase the risk for SLE. Our results do not support such hypothesis. Our findings suggest that linkage between SLE and the 18q21–23 region is due to a gene other than Bcl-2.
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Support: The project is supported by the European Commission grant BMH4–98–3489, the Nordic Academy for Advanced Study grant 00.15.062-O and the Consejo Nacional de Ciencia y Tecnología, Mexico and by the following grants awarded to MEAR: The Swedish Medical Research Council (No. 12673), The Åke Wibergs Stiftelse, The King Gustaf V:80th Birthday Fund and The Swedish Association against Rheumatism. CJ is supported by the Inflammation Program of the Swedish Foundation for Strategic Research Graduate Student program granted to MEAR. Support has also been obtained from the Swedish Medical Research Council to GS (13489), the Swedish Association against Rheumatism, the King Gustaf V:80th Birthday Fund and the Margareta Rheumatology Research Foundation to IL.
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Johansson, C., Castillejo-López, C., Johanneson, B. et al. Association analysis with microsatellite and SNP markers does not support the involvement of BCL-2 in systemic lupus erythematosus in Mexican and Swedish patients and their families. Genes Immun 1, 380–385 (2000). https://doi.org/10.1038/sj.gene.6363688
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DOI: https://doi.org/10.1038/sj.gene.6363688
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