Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Science. 2011 Jul 22;333(6041):405; author reply 405. doi: 10.1126/science.1198277.
Manicassamy et al. (Reports, 13 August 2010, p. 849) deleted β-catenin in intestinal immune cells using a CD11c-driven Cre recombinase, which decreased anti-inflammatory mediators and increased inflammatory bowel disease. However, the deletion of β-catenin in macrophages remains a caveat to their interpretation that Wnt signaling programs dendritic cells into a tolerogenic state. Development of strains expressing Cre in a more finely lineage-restricted pattern may help resolve this issue.
马尼卡萨米等人（2010 年 8 月 13 日，第 849 页）在肠道免疫细胞中使用 CD11c 驱动的 Cre 重组酶删除 β-连环蛋白，从而减少抗炎介质并增加炎症性肠病。然而，巨噬细胞中 β-连环蛋白的缺失仍然是他们的解释中的一个警告，即 Wnt 信号通路将树突状细胞编程为耐受状态。表达 Cre 的菌株在更精细的谱系限制模式下的发展可能有助于解决这个问题。
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