A Possible Role of Serum Soluble TNF-related Apoptosis-Inducing Ligand (TRAIL) in Pathogenesis of Systemic Lupus Erythematosus

The present study aimed to estimate the serum levels of soluble tumor necrosis factor-related apoptosis-inducing ligand (sTRAIL) in patients with systemic lupus
erythematosus (SLE) and to compare these levels to that estimated in patients with
other autoimmune diseasesand to control levels. The study included 50 patients with
SLE underwent clinical and laboratory evaluation. Disease activity was determined
according to the SLE disease activity index (SLEDAI score; ≤4: inactive & >4: active
disease). The study also included 30 patients with diagnosed rheumatoid arthritis
(RA, n=15) and Wegener’s granulomatosis (WG, n=15) and 10 healthy volunteers as
control group. All study participants gave blood samples for ELISA estimation of
serum sTRAIL concentration. The Clinical evaluation of SLE patients defined 27
patients with inactive and 23 patients with active SLE with mean SLEDAI score of
2±0.2 and 9.96±0.63, respectively. Mean blood levels of C3 and C4 were significantly
(p<0.001) decreased, while mean CRP level and anti-dsDNA antibodies levels were
significantly (p<0.001) higher in patients with active SLE compared to those with
inactive disease. Also, both total and differential leucocytic counts were significantly
lower in patients with active compared to those with quiescent disease and 5 patients
were neutropenic. Mean serum levels of sTRAIL were significantly higher in SLE
patients, irrespective to the disease activitycompared to serum levels estimated in
controls (P1=0.005) and in RA and WG patients (P2& P3=0.001). On contrary,
serum sTRAIL levels estimated in RA and WG were non-significantly higher
compared to control level (P1>0.05), also with a non-significantly higher levels in RA
patients compared to levels estimated in WG patients (P2>0.005). Patients with
inactive SLE had a significantly (P4=0.002) higher serum levels of sTRAIL compared
to levels estimated in patients with active SLE. Serum sTRAIL showed a negative
significant correlation with SLEDAI score and laboratory parameters of SLE activity.
Conclusion: It could be concluded that TRAIL has a possible role in pathogenesis
and initiation of activity of SLE and estimation of serum sTRAIL could be used as a
specific marker for differentiation betweenSLE from other autoimmune diseases and
between patients with active and inactive disease.