Human Molecular Genetics Advance Access published online on January 8, 2008
Human Molecular Genetics, doi:10.1093/hmg/ddn004
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Genetic Variation in the CRP Promoter: Association with Systemic Lupus Erythematosus (SLE)
1 Division of Clinical Immunology and Rheumatology, Department of Medicine 2 Section on Statistical Genetics and Bioinformatics, Department of Biostatistical Sciences, Division of Public Health Sciences, Wake Forest University, Winston-Salem, NC 3 Department of Epidemiology and University of Alabama at Birmingham, Birmingham, AL 4 Section of Trauma, Burns, and Critical Care, Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 5 Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD 6 Division of Rheumatology, Northwestern University School of Medicine, Chicago, IL 7 Division of Rheumatology, Department of Medicine, University of Texas Health Science Center at Houston, Houston, TX 8 Oklahoma Medical Research Foundation, Oklahoma City, OK 9 US Department of Veteran Affairs, Oklahoma City, OK and Department of Medicine, University of Oklahoma, Oklahoma City, OK
* Address for correspondence and reprints: Dr. Jeffrey C. Edberg, Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, SHEL207, 1825 University Blvd, Birmingham, AL 35294-2182. Phone: 205-934-0894, Fax: 205-996-6734. E-mail: jedberg{at}uab.edu
Received October 9, 2007; Revised December 22, 2007; Accepted January 4, 2008
The pentraxin C-reactive protein (CRP), an innate immune system opsonin which binds nuclear debris and apoptotic bodies, may protect against autoimmunity. A relative deficiency of CRP levels in patients with systemic lupus erythematosus (SLE) might contribute to altered handling of self antigens. We report that the proximal 5’ promoter region of CRP contains several polymorphisms that exhibit association with SLE in multiple populations. Strongest association was observed at the proximal promoter SNP rs3093061 (CRP-707)(p=6.41x10–7 and p=2.13x10–6 in African-American and Caucasian case-control samples respectively). This association remains after adjustment for admixture. Linkage disequilibrium exists between SNPs in the proximal promoter and association of functional haplotypes containing rs3091244/rs3093062 (CRP-409/-390) appear to be driven by the rs3093061 (CRP-707) association. These data demonstrate that rs3093061 at the -707 site within the CRP gene is an SLE susceptibility locus.
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