Induction of Systemic Lupus Erythematosus-like Syndrome in BALB/c Mice Leads to Disturbance in Splenic T Cell Subpopulations

Mechanisms underlying the systemic lupus erythematosus (SLE) have not yet been elucidated. In this study, we evaluated the balance of T cell subsets in BALB/c mice model of SLE induced; using Con A and polyamines as DNA immunogenicity modifiers. BALB/c mice were immunized subcutaneously with 50 µ𝑔 extracted DNA from cells cultured in different conditions: splenocytes+ polyamines (group P), splenocytes+ Con A (group A), splenocytes+ polyamines+ Con A (group PA) and splenocytes only (control). Anti-double-stranded DNA-(dsDNA) antibodies, proteinuria, and antinuclear autoantibodies were assessed by enzymelinked immunosorbent assay, Bradford method, and immunofluorescence respectively. Transcription factors of different T helper subsets were examined by realtime polymerase chain reaction. The serum level of the anti-dsDNA antibody in group PA was higher than that in the other groups (p 0.05). Antinuclear antibody (ANA) titer increased in groups A and PA. Proteinuria level in group PA was significantly higher than that in the control group (p 0.001). Expression of Foxp3 was decreased in group A (p=0.001). Additionally, the ratios of T-bet/GATA3 andthe T-bet/Foxp3 were also increased in group A. (p 0.05). Our results revealed an increased ratio of Th1 to Th2 and decreased expression of Foxp3 in group A, but group PA manifested more obvious signs of the disease. These results suggest that other mechanisms rather than disturbance in T cells balance may involve the development of disease symptoms.