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FRI0424 Role of IL-10 Gene Polymorphism and C1q Antibodies in Clinicopathological Presentations and Treatment Response in Lupus Nephritis Patients
  1. M. Tayel1,
  2. A. El zawawy1,
  3. M. Ibrahim2,
  4. E. Waked3,
  5. S. El Gendy4,
  6. S. Abdel Razek3
  1. 1Internal Medicine
  2. 2Clinincal Pathology, Alexandria Faculty of Medicine, Alexandria
  3. 3Internal Medicine, Teodor Bilharz Research, Menoufia
  4. 4Pathology, Alexandria Faculty of Medicine, Alexandria, Egypt


Background Defining an early and reliable and non invasive biomarker of kidney involvement in SLE is highly desirable. Anti-C1q auto antibodies have been proposed as a useful marker in SLE since their occurrence correlates with renal involvement and, possibly, with nephritic activity.

Interleukin-10 (IL-10), is a multifunctional cytokine that plays a crucial role in inflammation and the immune system. High IL-10 expression and the corresponding IL-10 alleles have been suggested to play a causal or exacerbating role in SLE. The promoter of the IL-10 gene is highly polymorphic, IL-10 gene-A/C polymorphism may play a role in the clinical and pathological diversity of lupus nephritis

Objectives evaluate the prevalence of anti-C1q antibodies in patients with SLE, with and without renal involvement, and to correlate it with the activity of the disease. Secondly, to investigate the -592 A/C polymorphism in patients with lupus nephritis and to assess its influence on IL-10 secretion in vivo

Methods 60 SLE patients were recruited in the study, and they were divided into 2 groups, group1, 40 patients with biopsy proven lupus nephritis and group 2, 20 SLE patients without nephritis. Sera were tested for anti-C1q, and IL-10 by enzyme immunoassay. IL-10 gene -592 A/C polymorphism by real time PCR. Frequencies of the genotypes were compared between the two groups

Results Anti-C1q antibodies were found to be significantly higher in patients with active lupus nephritis than those without nephritis with a median of 59.52±56.59 (p=0.001**). In those with active lupus nephritis, anti-C1q was found to correlate significantly with other parameters assessing lupus nephritis activity like C3 (p=0.011*), ESR (p=0.019), anti-dsDNA (p=0.011*), creatinine clearance (p=0.011*), and proteinuria (p=0.006**). No significant differences were found in the distribution of the polymorphism between lupus nephritis and those without nephritis. AC/CC genotypes were more frequent in patients with LN- III and IV than in those with LN class V. There was no significant difference in the serum IL-10 levels in patients with these three genotypes.

Conclusions Anti-C1q antibodies may serve as potential reliable and non invasive marker of SLE disease activity and renal involvement to avoid unnecessary renal biopsies. The IL-10 gene –592 A/C polymorphism appears to be associated and renal pathology of LN, but not associated with serum IL-10 levels. Patients carrying the –592 C allele had a higher risk of proliferative glomerulonephritis, indicating the genetic influence of the IL-10 gene polymorphism in the renal lesions of LN.


  1. Pickering MC, Botto M, Taylor PR, et al.: systemic lupus erythematosus, complement deficiency, and apoptosis. Adv Immunol 2000;76:227-334.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.1060

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