Li, Jintao Zhang, Ji Guo, Hongxia Yang, Shimin Fan, Weiping Ye, Nan Tian, Zhiqiang Yu, Tiantian Ai, Guoping Shen, Zigang He, Haiyang Yan, Ping Lin, Hui Luo, Xue Li, Hongli Wu, Yuzhang Image_11_Critical Role of Alternative M2 Skewing in miR-155 Deletion-Mediated Protection of Colitis.tiff <p>Inflammatory bowel disease (IBD) is associated with dysregulation of both innate and adaptive immune response in the intestine. MicroRNA (miR)-155 is frequently expressed and functions in many immune cell types. Besides its function in adaptive immunity, miR-155 is a key regulator of the innate immune response in macrophages, dendritic cells, and even in epithelia cells. Although the roles of miR-155 within T and B lymphocytes in colitis have been reported, its function in innate immune cells has not been thoroughly examined. In this study, the dextran sulfate sodium (DSS)-induced colitis model was established in wild-type (WT) and miR-155<sup>−/−</sup> mice. Our results showed that miR-155 deficiency in macrophages recapitulated the alleviated colitis feature of miR-155<sup>−/−</sup> mice and appeared to skew toward the alterative M2 phenotype. Notably, the predominance of M2 in colon can result in dampened intestinal immune cell proliferation and inhibit CD4 T cell polarization toward Th1 and Th17. Moreover, C/EBPβ and SOCS1 were demonstrated as two key functional targets in this process. We also provided evidence for use of miR-155 inhibitor to treat colitis. Collectively, the findings highlight the central role of alternative M2 skewing for miR-155 function in colitis and reveal that macrophages might be a main target for therapeutics.</p> M2 macrophages;miR-155;colitis;C/EBPβ;SOCS1 2018-05-03
    https://frontiersin.figshare.com/articles/figure/Image_11_Critical_Role_of_Alternative_M2_Skewing_in_miR-155_Deletion-Mediated_Protection_of_Colitis_tiff/6214424
10.3389/fimmu.2018.00904.s003