Université Européenne de Bretagne, France.
J Autoimmun. 2011 Nov;37(3):190-7. doi: 10.1016/j.jaut.2011.05.014.
One way for intravenous Ig (IVIg) to affect responses of the B cells might be to operate through their TLR7 and TLR9. We confirm the ability of TLR agonists to induce CD25 expression in B cells. For this to occur, sialylated Fc-gamma of IgG included in the IVIg preparation are required. As a result, IVIg suppresses TLR-induced production of the proinflammatory IL-6, but not that of the anti-inflammatory IL-10. That is, IVIg mimics the effects of the MyD88 inhibitor. Finally, as we previously showed that IVIg induces CD22 to recruit the inhibitory SHP-1, we established that this enzyme was also involved in IVIg-induced inhibition of TLR9 signaling. This is the first report to demonstrate such a mechanism underlying the negative impact of IVIg on B lymphocytes.
静脉注射免疫球蛋白（IVIg）影响 B 细胞反应的一种方式可能是通过其 TLR7 和 TLR9 发挥作用。我们证实了 TLR 激动剂诱导 B 细胞表达 CD25 的能力。为了实现这一点，IVIg 制剂中包含的 IgG 的唾液酸化 Fc-γ 是必需的。结果，IVIg 抑制 TLR 诱导的促炎细胞因子 IL-6 的产生，但不抑制抗炎细胞因子 IL-10 的产生。也就是说，IVIg 模拟了 MyD88 抑制剂的作用。最后，正如我们之前表明的那样，IVIg 诱导 CD22 招募抑制性 SHP-1，我们确定该酶也参与了 IVIg 诱导的 TLR9 信号转导抑制。这是首次报道证明 IVIg 对 B 淋巴细胞的负面影响存在这样的机制。
