Systemic lupus erythematosus (SLE) is an inflammatory rheumatic disease characterized by production of autoantibodies and organ damage. Elevated levels of cytokines have been reported in SLE patients. In this study we have investigated the effect of proinflammatory cytokines (IL-6, TNF-α, and IL-1β) on clinical manifestations in 145 Indian SLE patients. One hundred and forty-five healthy controls of the same ethnicity served as a control group. Clinical disease activity was scored according to SLEDAI score. Accordingly, 110 patients had active disease and 35 patients had inactive disease. Mean levels of IL-6, TNF-α, and IL-1β were found to be significantly higher in SLE patients than healthy controls (P < 0.001). Mean level of IL-6 for patients with active disease (70.45±68.32 pg/mL) was significantly higher (P = 0.0430) than those of inactive disease patients (43.85±63.36 pg/mL). Mean level of TNF-α was 44.76±68.32 pg/mL for patients with active disease while it was 25.97±22.03 pg/mL for those with inactive disease and this difference was statistically significant (P = 0.0161). Similar results were obtained for IL-1β (P = 0.0002). Correlation between IL-6, TNF-α, and IL-1β serum levels and SLEDAI score was observed (r = 0.20, r = 0.27, and r = 0.38, resp.). This study supports the role of these proinflammatory cytokines as inflammatory mediators in active stage of disease.

Epstein-Barr viral infection is one of the known environmental factors involved in development of Systemic Lupus Erythematous (SLE). Though not much is known about the exact role of Epstein-Barr virus (EBV) in SLE pathogenesis, the theory of switching of lytic and lysogenic cycles of EBV in memory B cells fits well with the periods of waning disease activity and intermittent flares in SLE patients. In this study, we investigate the association of EBV antibody profile with clinical and serological parameters in SLE. Eighty-seven clinically diagnosed SLE patients fulfilling the American College of Rheumatology (ACR) classification criteria and fifty healthy individuals were enrolled in this case control study. Anti-VCA IgM, anti-VCA IgG, and anti-EBNA IgG were detected by ELISA technique. Antibodies concentrations between two groups were compared using Mann-Whitney whereas the difference in categorical data was compared using Chi-square considering statistical significance at P < 0.05. This study demonstrated a significant increase in EBV VCA-IgG, VCA-IgM, and EBNA-IgG antibodies levels of SLE patients when compared to healthy controls (P < 0.05). High seroprevalence was seen in both the study groups for EBV VCA-IgG and EBNA-IgG antibodies when compared to VCA-IgM antibodies. A significant increase was noted in the anti-VCA-IgG levels with dsDNA autoantibody positivity (P < 0.05). Though there was no significant association between EBV antibody profile and clinical manifestations, 100% seropositivity for anti-VCA-IgG was seen in SLE patients with renal manifestations. Association of anti-VCA IgG levels with presence of anti-dsDNA antibodies suggests a possible role of EBV as an environmental trigger in pathogenesis of SLE.

In a cohort of 70 systemic lupus erythematosus (SLE) patients diagnosed over 2 years period, 14 patients were found to have confirmed antecedent tuberculosis (20.0%) which was 40 times higher (p < 0.001, 95%CI 36.2-48.6) than the prevalence of tuberculosis in the local population. Demonstration of anti-histone antibodies in similar proportion of SLE patients with and without antecedent anti-TB treatment and similar proportion of renal involvement (36 vs. 40%) between anti-TB drug exposed and non-exposed patients ruled out the drugs to be causative factors in precipitating SLE in these patients with antecedent history of tuberculosis. A cohort of 30 confirmed pulmonary tuberculosis patients were also studied in parallel to demonstrate high incidence of autoantibodies in these patients but no SLE. This study suggests a role of prior tuberculosis in precipitating SLE in genetically predisposed patients.

Anti-nuc antibody detection could be a better tool for the diagnosis of SLE. Although there was no significant difference in LN and SLE without LN groups, this study suggests that anti-nuc detection can be useful as an additional disease activity marker to other laboratory tests.