Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Postdoctoral Research Associate Program, National Institute of General Medical Sciences, National Institutes of Health, Bethesda, MD 20892, USA.
Immunity. 2021 Mar 9;54(3):514-525.e6. doi: 10.1016/j.immuni.2021.02.015. Epub 2021 Mar 2.
MicroRNAs are important regulators of immune responses. Here, we show miR-221 and miR-222 modulate the intestinal Th17 cell response. Expression of miR-221 and miR-222 was induced by proinflammatory cytokines and repressed by the cytokine TGF-β. Molecular targets of miR-221 and miR-222 included Maf and Il23r, and loss of miR-221 and miR-222 expression shifted the transcriptomic spectrum of intestinal Th17 cells to a proinflammatory signature. Although the loss of miR-221 and miR-222 was tolerated for maintaining intestinal Th17 cell homeostasis in healthy mice, Th17 cells lacking miR-221 and miR-222 expanded more efficiently in response to IL-23. Both global and T cell-specific deletion of miR-221 and miR-222 rendered mice prone to mucosal barrier damage. Collectively, these findings demonstrate that miR-221 and miR-222 are an integral part of intestinal Th17 cell response that are induced after IL-23 stimulation to constrain the magnitude of proinflammatory response.
微小 RNA 是免疫反应的重要调节因子。在这里,我们展示了 miR-221 和 miR-222 调节肠道 Th17 细胞反应。miR-221 和 miR-222 的表达被促炎细胞因子诱导,并被细胞因子 TGF-β 抑制。miR-221 和 miR-222 的分子靶标包括 Maf 和 Il23r,并且 miR-221 和 miR-222 的缺失使肠道 Th17 细胞的转录组谱向促炎特征转变。尽管 miR-221 和 miR-222 的缺失可以容忍维持健康小鼠肠道 Th17 细胞的内稳态,但缺乏 miR-221 和 miR-222 的 Th17 细胞在响应 IL-23 时更有效地扩增。miR-221 和 miR-222 的全局和 T 细胞特异性缺失使小鼠更容易发生黏膜屏障损伤。总之,这些发现表明,miR-221 和 miR-222 是肠道 Th17 细胞反应的一个组成部分,在 IL-23 刺激后被诱导,以限制促炎反应的幅度。