成纤维细胞通过胰岛素样生长因子1调控固有淋巴细胞抑制肠道炎症
Fibroblasts restrain gut inflammation by IGF1-dependent regulation of innate lymphocytes
炎症性肠病患者肠道中一类表达胰岛素样生长因子1的成纤维细胞减少，这类细胞如何影响免疫结果此前并不清楚。研究者用小鼠肠道炎症模型发现，该成纤维细胞与3型固有淋巴细胞存在相互作用；胰岛素样生长因子1刺激会限制固有淋巴细胞产生趋化因子CXCL10，从而减少浆细胞样树突状细胞的募集，抑制肠道炎症。作者认为这一调控通路在人类固有淋巴细胞中保守，但在炎症性肠病中可能受损，提示抗炎成纤维细胞是保护肠道的潜在靶点。
为什么推荐给您：揭示成纤维细胞-固有淋巴细胞-树突状细胞新调控轴，具转化前景但尚属机制研究。
不需要生物学背景，多打比方
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摘要Abstract
Fibroblasts exhibit phenotypic and functional heterogeneity in chronic inflammatory diseases, but how these changes impact immune outcomes remains poorly understood. We identified that a fibroblast population expressing insulin-like growth factor 1 (IGF1) was reduced in patients with inflammatory bowel disease (IBD). Using mouse models of intestinal inflammation, we found cross-talk between IGF1-expressing fibroblasts and group 3 innate lymphoid cells (ILC3s). IGF1 stimulation limited the ability of ILC3s to produce C-X-C motif chemokine ligand 10 (CXCL10) and recruit plasmacytoid dendritic cells (pDCs) to restrain gut inflammation. We propose that this regulatory pathway is conserved in human ILC3s but may become impaired in IBD. Our results define that anti-inflammatory fibroblasts safeguard the gut through regulation of an innate lymphocyte-pDC axis.