Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of autoantibodies against nucleic acid-associated antigens. B cells play cardinal roles in SLE. Many evidences have proved estrogen contribute to the gender bias in SLE and 17β-estradiol (E2) could accelerate the disease by regulating B cells. On the other hand, B cells express TLR9 which recognized dsDNA and played a critical role in SLE. However, the crosstalk between estrogen and TLR9 in B cells remains unknown. So we investigated the E2 effect in the presence of the TLR9 ligand CpG on mice spleen B cells. We found that the up-regulation of cell viability, life-span, co-stimulation molecules (CD40, CD86) expression, IgM secretion, TLR9 and MCM6 expression were more significant than CpG ODN or E2 stimulated alone. It may provide a new way to investigate the mechanism of how E2 modulate the B cells function in lupus.
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