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Volume 3 Supplement 2

21st European Workshop for Rheumatology Research

  • Meeting abstract
  • Open Access

Elevated IL-16 level is a non-genetic characteristic of patients with severe systemic lupus erythematosus

  • 1,
  • 2 and
  • 1
Arthritis Research & Therapy20013 (Suppl 2) :P016

https://doi.org/10.1186/ar185

  • Received: 15 January 2001
  • Published:

Keywords

  • Systemic Lupus Erythematosus
  • Healthy Volunteer
  • Disease Severity
  • Degree Relative
  • Organ Damage

Introduction

IL-16, origanilly named lymphocyte chemoattractant factor, is a cytokine which is mainly produced by CD8+ T cells. Several reports have described that increased levels of IL-16 are in part responsible for T cell abnormalities in SLE patients. It is unknown if the previously reported increased levels of IL-16 is a characteristic underlying susceptibility to SLE or is a characteristic of the disease itself.

Methods

Accumulated organ damage was measured with the SLICC/ACR Damage Index. Twenty-five severe (SLICC/ACR: 4.9 ± 2.5) and ten non-severe (SLICC/ACR: 1.0 ± 0.8) SLE patients were included in this study. Also 11 first degree relatives and 12 healthy volunteers were included in this study. Plasma IL-16 levels were measured by ELISA.

Results

No significant difference in the IL-16 levels of the first degree relatives of patients with SLE (38.3 ± 11.1 pg/ml) were observed when compared to controls (31.2 ± 10.1 pg/ml). In order to analyze characteristics of the SLE in relation to concentration of IL-16, IL-16 was measured in severe SLE patients (71.3 ± 87.4 pg/ml; P = 0.025) compared to healthy controls. On the other hand, no significant differences were observed between the non-severe SLE patients (37.8 ± 26.1 pg/ml) and controls.

Conclusion

No evidence for increased IL-16 levels in first degree relatives of the SLE patients was observed. IL-16 is enhanced in SLE patients with a severe disease, but not in patients with non-severe disease, thereby suggesting that IL-16 is associated with disease severity, and not with susceptibility for SLE.

Authors’ Affiliations

(1)
Departments of Rheumatology and Immunohaematology, The Netherlands
(2)
Bloodbank, Leiden University Medical Center, Leiden, The Netherlands

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