标题：Deletion of miRNAs in bone marrow prevents streptozotocin-induced murine autoimmune diabetes but deletion of miR-155 does not
作者机构：[Chen, W.-B] Institute of Pharmacology, Shandong University School of Medicine, Jinan, China, Henry Ford Immunology Program, Henry Ford Health System, 更多
通讯作者地址：[Mi, QS]Henry Ford Hlth Syst, Henry Ford Immunol Program, Detroit, MI USA.
摘要：Recent studies have demonstrated that gene expression is regulated not only by protein-coding genes, but also by non-protein-coding RNA molecules, including microRNAs (miRNAs). miRNAs are a class of 21-25 nt single-stranded non-coding small RNAs dependent upon ribonuclease III enzyme Dicer for the processing of mature and functional miRNAs. Therefore, the deletion of the enzyme Dicer provides a genetic test for the relevance of miRNAs in mammalian development and function. We and others previously reported that loss of miRNAs in bone marrow induced by Tie2-Cre or in thymus by CD4-Cre, through tissue-specific deletion of miRNA-dependent Dicer, mainly regulated the development and function of CD4~+CD25~+Foxp3~+ regulatory T (Treg) cells and invariant natural killer T (iNKT) cells, but did not affect conventional CD4 and CD8 T cell development in the thymus.