To evaluate the serum level of soluble glycoprotein-130 (sgp130), Monocyte Chemotactic Protein-3 (MCP3) and soluble-leptin-receptor (SLR)in with systemic lupus erythematosus (SLE-patients) as a prototype and major systemic autoimmune disease and its relationship with various variables. 50 variables besides the sgp130, MCP3 and SLR were evaluated. The results of the comparison of sgp130, MCP3 and SLR between two groups showed that only the difference related to SLR was statistically significant.It was also revealed that patients had higher level of anti-nuclear antibodies (ANA), antidouble- stranded DNA antibodies (anti-dsDNA), C-reactive-protein (CRP), erythrocyte-sedimentationrate (ESR), but lower C3, C4, hemoglobin (Hb) and hematocrit (Hct) than controls. However no significant differences for socio-demographic or lifestyle parameters were found between patients and controls but depression status and its prevalence in the patients was higher than controls. We showed that depression of SLE-patients correlate positively with ANA and some habits like, alcohol, cigarette and hookah consumption. Although there was no significant difference between weights, patients had significantly lower SLR level after adjustment for other variables. A negative correlation was also found between SLR level with weight (in both groups) and depression (in patients). We also showed that higher weight is associated with higher anti-dsDNA titer in SLE-patients.Finally, we emphasized on several risk factors for SLE including overweight, depression and smoking which may be harmful for SLE-patients. For the first time, this study indicated a lower level of SLR,despite a similar MCP3 and sgp130 in SLEpatients and also investigated the relationship between these moleculesand 50 different variables. The negative correlation of patient’s SLR level with the patient’s weight or depression score, together with the lower SLR level in patients than in controls indicate that lower concentration of SLR in these patients, may be implicated in the pathogenesis of SLE.
