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首页> 外文期刊>Cellular immunology >17β-Estradiol enhances response of mice spleen B cells elicited by TLR9 agonist
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17β-Estradiol enhances response of mice spleen B cells elicited by TLR9 agonist

机译：17β-雌二醇可增强TLR9激动剂引起的小鼠脾脏B细胞的应答

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摘要

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.
机译：系统性红斑狼疮（SLE）是一种自身免疫性疾病，其特征是产生针对核酸相关抗原的自身抗体。 B细胞在SLE中起主要作用。许多证据证明雌激素会导致SLE中的性别偏见，而17β-雌二醇（E2）可以通过调节B细胞来加速疾病的发展。另一方面，B细胞表达可识别dsDNA的TLR9，并在SLE中起关键作用。但是，B细胞中雌激素和TLR9之间的串扰仍然未知。因此，我们研究了在TLR9配体CpG存在下对小鼠脾B细胞的E2效应。我们发现细胞活力，寿命，共刺激分子（CD40，CD86）表达，IgM分泌，TLR9和MCM6表达的上调比单独刺激CpG ODN或E2更重要。它可能为研究E2如何调节狼疮中B细胞功能的机制提供新途径。

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