Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Nat Commun. 2014 Mar 17;5:3495. doi: 10.1038/ncomms4495.
Here, we test the role of FoxP3(+) regulatory T cells (Tregs) in controlling T follicular helper (Tfh) and germinal centre (GC) B-cell responses to influenza. In contrast to the idea that Tregs suppress T-cell responses, we find that Treg depletion severely reduces the Tfh cell response to influenza virus. Furthermore, Treg depletion prevents the accumulation of influenza-specific GCs. These effects are not due to alterations in TGFβ availability or a precursor-progeny relationship between Tregs and Tfh cells, but are instead mediated by increased availability of IL-2, which suppresses the differentiation of Tfh cells and as a consequence, compromises the GC B response. Thus, Tregs promote influenza-specific GC responses by preventing excessive IL-2 signalling, which suppresses Tfh cell differentiation.
在这里,我们测试了 FoxP3(+)调节性 T 细胞(Tregs)在控制滤泡辅助性 T 细胞(Tfh)和生发中心(GC)B 细胞对流感的反应中的作用。与 Tregs 抑制 T 细胞反应的观点相反,我们发现 Treg 耗竭严重降低了对流感病毒的 Tfh 细胞反应。此外,Treg 耗竭可防止流感特异性 GC 的积累。这些影响不是由于 TGFβ可用性的改变或 Tregs 和 Tfh 细胞之间的前体-后代关系,而是通过增加 IL-2 的可用性来介导的,IL-2 抑制了 Tfh 细胞的分化,因此损害了 GC B 反应。因此,Tregs 通过防止过度的 IL-2 信号转导来促进流感特异性 GC 反应,从而抑制了 Tfh 细胞的分化。