Mechanisms and kinetics of proliferation and fibrosis development in a mouse model of thyrocyte hyperplasia

Radu Tudor Ciornei, So Hee Hong, Yujiang Fang, Ziwen Zhu, Helen Braley-Mullen

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


IFN-γ-/- 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 28 days, 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.

Original languageEnglish
Pages (from-to)16-26
Number of pages11
JournalCellular Immunology
StatePublished - 1 Jun 2016

Bibliographical note

Publisher Copyright:
© 2016 Elsevier Inc.


  • Autoimmunity
  • Fibrosis
  • Senescence
  • Thyrocyte proliferation
  • Thyroid epithelial cell (thyrocyte) hyperplasia


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