A fast antibody response can be critical to contain rapidly dividing pathogens. This can be achieved by the expansion of antigen-specific B cells in response to T-cell help followed by differentiation into plasmablasts. MicroRNA-155 (miR-155) is required for optimal T-cell-dependent extrafollicular responses via regulation of PU.1, although the cellular processes underlying this defect are largely unknown. Here, we show that miR-155 regulates the early expansion of B-blasts and later on the survival and proliferation of plasmablasts in a B-cell-intrinsic manner, by tracking antigen-specific B cells in vivo since the onset of antigen stimulation. In agreement, comparative analysis of the transcriptome of miR-155-sufficient and miR-155-deficient plasmablasts at the peak of the response showed that the main processes regulated by miR-155 were DNA metabolic process, DNA replication, and cell cycle. Thus, miR-155 controls the extent of the extrafollicular response by regulating the survival and proliferation of B-blasts, plasmablasts and, consequently, antibody production.

中文翻译：

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MicroRNA-155 对于浆母细胞 B 细胞的最佳增殖和存活至关重要。

快速的抗体反应对于遏制快速分裂的病原体至关重要。这可以通过响应于 T 细胞帮助而扩增抗原特异性 B 细胞然后分化为浆母细胞来实现。MicroRNA-155 (miR-155) 是通过调节 PU.1 实现最佳 T 细胞依赖性滤泡外反应所必需的，尽管这种缺陷背后的细胞过程在很大程度上是未知的。在这里，我们展示了 miR-155 通过在抗原刺激开始后在体内追踪抗原特异性 B 细胞，以 B 细胞固有的方式调节 B 母细胞的早期扩增，以及随后以 B 细胞固有的方式调节浆母细胞的存活和增殖。同意，miR-155-充足和miR-155-缺陷型浆母细胞在反应高峰时的转录组比较分析表明，miR-155调控的主要过程是DNA代谢过程、DNA复制和细胞周期。因此，miR-155 通过调节 B 母细胞、浆母细胞的存活和增殖，从而控制抗体的产生，来控制滤泡外反应的程度。