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Potential Viral Model for SLE: Accelerated Polyclonal Autoantibody Production Following Theiler

Byung S. Kim

Systemic lupus erythematosus (SLE) is caused by the production of antibodies against self-antigens. The onset and/or progression of SLE appears to be associated with various viral infections. However, the underlying mechanisms of the association are not well understood due to the lack of suitable infectious experimental models. Recently, we demonstrated that a wide range of B cells are permissive to Theiler’s murine encephalomyelitis virus (TMEV), and TMEV-infected B cells are activated to up regulate co-stimulatory molecules for T cell stimulation. The initial activation of B cells requires the production of IFN-α/β.Subsequently produced IFN-α/β, IL-6, and IL-1 facilitate further B cell activation for antibody production and skewed development of Th17 type response. When SLE-prone BXSB and NZBWF1 mice were infected with TMEV and Coxsackie virus, the production of a wide range of autoantibodies in these autoimmune-prone mice was markedly accelerated. Several TLRs upon viral infections may participate in the B cell activation via NF-ҡB and critical cytokines such as IFN-α/β, IL-1, and IL-6. Therefore, TMEV infection in susceptible mice may offer an important tool to investigate the underlying mechanisms associated with B cell activation and consequent autoantibody production involved in SLE here.