Abstract
Objective
The objective of this study was to investigate whether hepatitis B virus (HBV) infection plays a role in the regulation of autoimmunity for systemic lupus erythematosus (SLE).
Method
A total of 21 female BALB/c mice and 21 female HBV transgenic BALB/c mice aged two months were randomly divided into four groups: BALB/c mice, HBVTg mice, pristane-injected BALB/c mice, and pristane-injected HBVTg mice. BALB/c mice and HBVTg mice were given an intraperitoneal injection of 0.5 ml normal saline, and the mice in the other two groups were given an intraperitoneal injection of 0.5 ml pristane. ANA and anti-dsDNA levels in serum were detected by indirect immunofluorescence. Interleukin 2 (IL-2), IL-4, IL-6, IL-17, and TNF-α were measured by Luminex technology. The serum BAFF level was measured using an Elisa kit. Twenty-four weeks after pristane administration, kidneys were removed, dissected, and stained with hematoxylin and eosin and periodic-acid Schiff.
Result
At six months after injecting, the ANA titers in pristane-injected HBVTg mice were significantly lower than pristane-injected BALB/c mice. IL-17, TNF-α, and BAFF levels were significantly higher in pristane-injected BALB/c mice than BALB/c mice and pristane-injected HBVTg mice. IL-2, IL-4, and IL-6 levels were much higher in pristane-injected HBVTg mice than pristane-injected BALB/c mice. In pristane-injected HBVTg mice and HBVTg mice, fewer glomerulonephritis changes were found in the kidneys.
Conclusions
Our results showed that the incidence of SLE was much lower in HBVTg mice, and that HBV infection helped the SLE mice survive high levels of inflammatory cytokines and severe renal damage. All these findings demonstrated the protective role of HBV in SLE patients via the immunoregulatory networks of the cytokines.
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