کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2167204 | 1549410 | 2012 | 11 صفحه PDF | دانلود رایگان |
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.
► E2 improved the viability and survival of B cells with TLR9 agonist CpG.
► E2 enhanced the activation and function of B cells with the treatment of CpG.
► In vivo experiments showed the similar results to in vitro studies.
► Expression of TLR9 and MCM6 involved in this regulation by E2 and CpG.
Journal: Cellular Immunology - Volume 278, Issues 1–2, July–August 2012, Pages 125–135