| First Author | Yu S | Year | 2006 |
| Journal | Clin Immunol | Volume | 118 |
| Issue | 1 | Pages | 92-100 |
| PubMed ID | 16150647 | Mgi Jnum | J:107231 |
| Mgi Id | MGI:3620437 | Doi | 10.1016/j.clim.2005.07.013 |
| Citation | Yu S, et al. (2006) Thyroid epithelial cell hyperplasia in IFN-gamma deficient NOD.H-2h4 mice. Clin Immunol 118(1):92-100 |
| abstractText | The role of inflammatory cells in thyroid epithelial cell (thyrocyte) hyperplasia is unknown. Here, we demonstrate that thyrocyte hyperplasia in IFN-gamma-/- NOD.H-2h4 mice has an autoimmune basis. After chronic exposure to increased dietary iodine, 60% of IFN-gamma-/- mice had severe thyrocyte hyperplasia with minimal or moderate lymphocyte infiltration, and thyroid dysfunction with reduced serum T4. All mice produced anti-thyroglobulin autoantibody. Some wild-type NOD.H-2h4 mice had isolated areas of thyrocyte hyperplasia with predominantly lymphocytic infiltration, whereas IL-4-/- and 50% of wild-type NOD.H-2h4 mice developed lymphocytic thyroiditis but no thyrocyte hyperplasia. Both thyroid infiltrating inflammatory cells and environmental factors (iodine) were required to induce thyrocyte hyperplasia. Splenocytes from IFN-gamma-/- mice with thyrocyte hyperplasia, but not splenocytes from naive IFN-gamma-/- mice, induced hyperplasia in IFN-gamma-/- NOD.H-2h4.SCID mice. These results may provide clues for understanding the mechanisms underlying development of epithelial cell hyperplasia not only in thyroids but also in other tissues and organs. |
