| First Author | Xu S | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 6764 | PubMed ID | 25881561 |
| Mgi Jnum | J:222711 | Mgi Id | MGI:5645416 |
| Doi | 10.1038/ncomms7764 | Citation | Xu S, et al. (2015) Mir-17-92 regulates bone marrow homing of plasma cells and production of immunoglobulin G2c. Nat Commun 6:6764 |
| abstractText | The polycistronic mir-17-92 cluster, also known as oncomir-1, was previously shown to be essential for early B lymphopoiesis. However, its role in late-stage B-cell differentiation and function remains unexplored. Here we ablate mir-17-92 in mature B cells and demonstrate that mir-17-92 is dispensable for conventional B-cell development in the periphery. Interestingly, mir-17-92-deficiency in B cells leads to enhanced homing of plasma cells to the bone marrow during T-cell-dependent immune response and selectively impairs IgG2c production. Mechanistically, mir-17-92 directly represses the expression of Sphingosine 1-phosphate receptor 1 and transcription factor IKAROS, which are, respectively, important for plasma cell homing and IgG2c production. We further show that deletion of mir-17-92 could reduce IgG2c anti-DNA autoantibody production and hence mitigate immune complex glomerulonephritis in Shp1-deficient mice prone to autoimmunity. Our results identify important roles for mir-17-92 in the regulation of peripheral B-cell function. |
