| First Author | Ciornei RT | Year | 2016 |
| Journal | Cell Immunol | Volume | 304-305 |
| Pages | 16-26 | PubMed ID | 27173733 |
| Mgi Jnum | J:345185 | Mgi Id | MGI:6822894 |
| Doi | 10.1016/j.cellimm.2016.04.006 | Citation | Ciornei RT, et al. (2016) Mechanisms and kinetics of proliferation and fibrosis development in a mouse model of thyrocyte hyperplasia. Cell Immunol 304-305:16-26 |
| abstractText | IFN-gamma(-/-) NOD.H-2h4 mice develop autoimmune disease with extensive hyperplasia and proliferation of thyroid epithelial cells (TEC H/P) and fibrosis. Splenic T cells from donors with severe TEC H/P transfer TEC H/P to SCID recipients. The goal of this study was to determine what factors control TEC H/P development/progression by examining T cells, markers of apoptosis, senescence and proliferation in thyroids of SCID recipients over time. At 28days, T cell infiltration was maximal, thyrocytes were proliferating, and fibrosis was moderate. At days 60 and 90, thyroids were larger with more fibrosis. T cells, cytokines and thyrocyte proliferation decreased, and cell cycle inhibitor proteins, and anti-apoptotic molecules increased. T cells and thyrocytes had foci of phosphorylated histone protein H2A.X, indicative of cellular senescence, when TEC H/P progressed and thyrocyte proliferation declined. Some thyrocytes were regenerating at day 90, with irregularly shaped empty follicles and ciliated epithelium. Proliferating thyrocytes were thyroid transcription factor (TTF1)-positive, suggesting they derived from epithelial cells and not brachial cleft remnants. |
