B Lymphocyte Stimulator (BLyS) Overexpression in Patients with Systemic Lupus Erythematosus, DINA R. BAHGAT, RASHA E. GHEITH and OLFAT SHAKER
Abstract
Members of the tumour necrosis factor (TNF) family induce pleiotropic biological responses, including cell growth, differentiation and even death. B lymphocyte stimulator (BLyS), a member of the tumour necrosis factor (TNF) super-family, is a cytokine that induces B-cell survival, expansion, and differentiation both in vitro and in vivo. Considerable evidence points to a role for (BLyS) overproduction in murine and human Systemic Lupus Erythematosus (SLE). Increased levels of BLyS mRNA correlates well with biologic and clinical sequelae of BLyS overexpression.
Aim of Work: To assess the level of mRNA BLyS in systemic lupus erythematosus patients and correlate it to clinical and laboratory features of the disease.
Material and Methods: Thirty SLE patients and ten age-and sex-matched healthy individuals were enrolled in the study. Blood samples from patients and controls were subjected to the following: Detection of BLyS mRNA expression by reverse transcriptase-polymerase chain reaction (RT-PCR) method, followed by semiquantitation of their levels by comparing levels of BLyS mRNA to ß-actin mRNA levels using densitometric analysis.
Results: The mean intensity of full-length BLyS mRNA expression was significantly higher in SLE patients when compared to the control group (p<0.001). Elevated BLyS mRNA in SLE patients are significantly associated with disease activity as they are statistically correlated with SLE disease activity index (SLEDAI) score. BLys mRNA levels were closely associated with serum anti-dsDNA levels and are not correlated to percentage of leucocyte lineages in the patients’ peripheral blood samples, denoting that among SLE patients, the elevated levels of BLyS mRNA are not related to percentage of myeloid lineage, they are expressed from.
Conclusion: BLyS mRNA levels may be a helpful biom-arker in the clinical monitoring of SLE patients. These findings also reinforces the rationale underlying clinical trials with BLyS antagonists in SLE.