Department of Immunology, Chiba University, Inohana, Chuo-ku, Chiba, Japan.
Department of Experimental Immunology, Chiba University, Inohana, Chuo-ku, Chiba, Japan.
PLoS One. 2021 Nov 22;16(11):e0260204. doi: 10.1371/journal.pone.0260204. eCollection 2021.
While IFNγ is a well-known cytokine that actively promotes the type I immune response, it is also known to suppress the type II response by inhibiting the differentiation and proliferation of Th2 cells. However, the mechanism by which IFNγ suppresses Th2 cell proliferation is still not fully understood. We found that IFNγ decreases the expression of growth factor independent-1 transcriptional repressor (GFI1) in Th2 cells, resulting in the inhibition of Th2 cell proliferation. The deletion of the Gfi1 gene in Th2 cells results in the failure of their proliferation, accompanied by an impaired cell cycle progression. In contrast, the enforced expression of GFI1 restores the defective Th2 cell proliferation, even in the presence of IFNγ. These results demonstrate that GFI1 is a key molecule in the IFNγ-mediated inhibition of Th2 cell proliferation.
虽然 IFNγ 是一种众所周知的细胞因子,可积极促进 I 型免疫反应,但它也通过抑制 Th2 细胞的分化和增殖来抑制 II 型反应。然而,IFNγ 抑制 Th2 细胞增殖的机制仍不完全清楚。我们发现 IFNγ 降低了 Th2 细胞中生长因子非依赖性-1 转录抑制因子(GFI1)的表达,从而抑制了 Th2 细胞的增殖。在 Th2 细胞中删除 Gfi1 基因会导致其增殖失败,并伴有细胞周期进程受损。相比之下,强制表达 GFI1 可恢复有缺陷的 Th2 细胞增殖,即使存在 IFNγ 也是如此。这些结果表明,GFI1 是 IFNγ 介导的抑制 Th2 细胞增殖的关键分子。