AI Article Synopsis
- High levels of miR-155 are linked to inflammatory bowel disease (IBD), with increased expression found in regulatory T (Treg) cells of patients.
- Mice overexpressing miR-155 in Treg cells develop autoimmune conditions and more severe intestinal damage when treated with DSS.
- MiR-155 impairs the production of Tfr and cTreg cells by targeting CTLA-4, which may lead to excessive B cell activation and contribute to serious intestinal injury seen in autoimmune IBD patients.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.intimp.2019.03.009 | DOI Listing |
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