scRNAseq of small intestine-derived lamina propria CD45+ cells from untreated wild type (WT), untreated intestinal epithelial specific LSD1 knockout (cKO), antibiotic-treated WT mice and antibiotic-treated cKO mice

Mice with an intestinal epithelial specific knockout of LSD1 have changes in the intestinal epithelium including loss of Paneth and Goblet cells along with a general status of epithelial immaturity. To assess the influence of these epithelial specific changes on the mucosal immune system we performed a scRNAseq on CD45+ immune cells from the small intestine of mice with an epithelial specific LSD1 deletion (Villin-Cre+; Lsd1f/f) and wild type mice (Villin-Cre -; Lsd1f/f). To rule out a possible influence of the bacterial microbiome in the observed changes in CD45+ cell types we performed the same experiment in mice treated with antibiotics. These data allowed us to pinpoint changes in the cell populations of the mucosal immune system upon loss of LSD1 in the intestinal epithelium such as IgA producing cells and ILCs.肠道上皮特异性敲除赖氨酸特异性去甲基化酶1（LSD1）的小鼠，其肠道上皮会出现一系列改变，包括潘氏细胞（Paneth cell）与杯状细胞（Goblet cell）的丢失，以及上皮整体未成熟的状态。 为评估这类上皮特异性变化对黏膜免疫系统的影响，我们对肠道上皮特异性LSD1缺失小鼠（Villin-Cre+; Lsd1f/f）及野生型小鼠（Villin-Cre-; Lsd1f/f）的小肠CD45阳性免疫细胞开展了单细胞RNA测序（scRNAseq）。 为排除细菌微生物组（bacterial microbiome）对所观测到的CD45阳性细胞群变化的潜在影响，我们在经抗生素处理的小鼠中重复了上述实验。 本数据集使得我们能够精准定位肠道上皮LSD1缺失后黏膜免疫系统细胞群的相关改变，包括免疫球蛋白A（IgA）分泌细胞与固有淋巴细胞（ILCs）。