First Author | Chao G | Year | 2019 |
Journal | Int Immunopharmacol | Volume | 71 |
Pages | 267-276 | PubMed ID | 30927737 |
Mgi Jnum | J:290924 | Mgi Id | MGI:6442836 |
Doi | 10.1016/j.intimp.2019.03.009 | Citation | Chao G, et al. (2019) MiR-155 controls follicular Treg cell-mediated humoral autoimmune intestinal injury by inhibiting CTLA-4 expression. Int Immunopharmacol 71:267-276 |
abstractText | High expression levels of miR-155 are involved in the pathogenesis of inflammatory bowel disease (IBD). We observed an increase in miR-155 in peripheral regulatory T (Treg) cells from IBD patients. Mice that specifically overexpress miR-155 in Foxp3+ Treg cells exhibit spontaneous autoimmunity and more severe dextran sulfate sodium (DSS)-induced intestinal injury. MiR-155 overexpression can lead to a lack of follicular Treg (Tfr) cells and central Treg (cTreg), whereas DSS treatment further depletes the Tfr cells. Furthermore, miR-155 can target the expression of CTLA-4 in cTreg and Tfr, directly inhibiting Tfr cell production and promoting enhanced germinal center (GC) B cell activation and autoantibody overproduction. This outcome may be the cause of severe intestinal injury in patients with autoimmune IBD. |