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  • Open Access

BAFF polymorphisms and serum levels of BAFF in Tunisian systemic lupus erythematosus patients

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Journal of Translational Medicine201210 (Suppl 3) :P35

  • Published:


  • Systemic Lupus Erythematosus
  • Systemic Lupus Erythematosus Patient
  • Regulatory Region
  • Autoantibody Production
  • Single Allele


Although different authors suggest that the B-lymphocyte activating factor (BAFF) may be involved in the selective loss of B-cell tolerance in human systemic lupus erythematosus (SLE), the mechanisms responsible for the deregulation of this molecule in SLE remain unclear [13].


To investigate any associations between regulatory genetic polymorphisms of BAFF gene, disease susceptibility and serum BAFF (s-BAFF) levels in Tunisian systemic lupus (SLE) patients.


The case-control study included 124 SLE patients and 152 healthy controls. Three single nucleotide polymorphisms (SNPs) (-2841 T>C, -2701 A>T and -871 C>T) in the 5’ regulatory region of the BAFF gene were explored by PCR-RFLP [4]. s-BAFF levels were measured by ELISA (R&D Systems).


s-BAFF levels were elevated in SLE patients (1717,08 pg/ml) and in anti-dsDNA positive antibodies patients (1948,28 pg/ml) compared to both controls (665,82 pg/ml, p<10-3) and patients without anti-dsDNA antibodies (1281,51 pg/ml, p:0,007). In contrast, no correlation was found between global disease activity registered in SLEDAI and s-BAFF levels (p: 0.7). Furthermore, no association was found between BAFF genotypes and susceptibility to SLE. Single allele, genotype and haplotype association analyses showed no significant association with s-BAFF values, clinical features or SLEDAI score in SLE.


Polymorphisms in the regulatory region of the BAFF gene do contribute neither to increased s-BAFF levels nor to the susceptibility to SLE in Tunisian patients. Increased s-BAFF levels in anti-dsDNA positive antibodies SLE patients suggest the central role of this molecule in the inflammatory process involving in autoantibodies production.

Authors’ Affiliations

Research Laboratory of Renal Transplantation and Immunopathology (LR03SP01), University Tunis El Manar, Charles Nicolle Hospital, Tunisia
Dept. of Medicine, Charles Nicolle Hospital, Tunis, Tunisia


  1. Becker-Merok A, Nikolaisen C, Nossent HC: B-lymphocyte activating factor in systemic lupus erythematosus and rheumatoid arthritis in relation to autoantibody levels, disease measures and time. Lupus. 2006, 15: 570-6. 10.1177/0961203306071871.View ArticlePubMedGoogle Scholar
  2. Zhang J, Roscheke V, Baker KP: A role of B lymphocyte stimulator in systemic lupus erythematosus. J Immunol. 2001, 166: 6-10.View ArticlePubMedGoogle Scholar
  3. Eilertsen G, Van Ghelue M, Strand H, Nossent J: Increased levels of BAFF in patients with systemic lupus erythematosus are associated with acute-phase reactants, independent of BAFF genetics: a case-control study. Rheumatology. 2011, 50: 2197-2205. 10.1093/rheumatology/ker282.View ArticlePubMedGoogle Scholar
  4. Nossent JC, Lester S, Zahra D: Polymorphism in the 5’regulatory region of the B-lymphocyte activating factor gene is associated with the RO/La autoantibody response and serum BAFF levels in primary Sjogren’s syndrome. Rheumatology. 2008, 47: 1311-6. 10.1093/rheumatology/ken246.View ArticlePubMedGoogle Scholar


© Laamiri et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.