| First Author | Esashi E | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 6 | Pages | 1664-70 |
| PubMed ID | 19384873 | Mgi Jnum | J:149482 |
| Mgi Id | MGI:3848588 | Doi | 10.1002/eji.200839149 |
| Citation | Esashi E, et al. (2009) Oncostatin M deficiency leads to thymic hypoplasia, accumulation of apoptotic thymocytes and glomerulonephritis. Eur J Immunol 39(6):1664-70 |
| abstractText | Oncostatin M (OSM) has been implicated in immune regulation, though its precise role remains elusive. Here we show that OSM plays a crucial role in the prevention of autoimmune diseases. OSM-deficient mice showed normal development of T cells, B cells and DC; however, their thymus showed hypoplasia and altered medullary structure. Autoantibodies against dsDNA accumulated and glomerulonephritis developed in aged OSM-deficient mice. Apoptotic cells accumulated in the thymus of OSM-deficient mice, and the administration of dexamethasone in young OSM-deficient mice resulted in the massive accumulation of apoptotic thymocytes and production of autoantibodies. These results suggest that OSM plays a key role in the prevention of autoimmune disease by regulating the clearance of apoptotic thymocytes. |
