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 Blood, 1 November 2008, Vol. 112, No. 9, pp. 3688-3695.
Prepublished online as a Blood First Edition Paper on August 11, 2008; DOI 10.1182/blood-2008-04-150532.

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IMMUNOBIOLOGY

Maintenance of a normal thymic microenvironment and T-cell homeostasis require Smad4-mediated signaling in thymic epithelial cells

Lukas T. Jeker1,*, Thomas Barthlott1,*, Marcel P. Keller1, Saulius Zuklys1, Mathias Hauri-Hohl1, Chu-Xia Deng2, and Georg A. Holländer1

1 Department of Biomedicine, Laboratory of Pediatric Immunology, University of Basel and the University Children's Hospital, Basel, Switzerland; and 2 Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD

Signals mediated by the transforming growth factor-β superfamily of growth factors have been implicated in thymic epithelial cell (TEC) differentiation, homeostasis, and function, but a direct reliance on these signals has not been established. Here we demonstrate that a block in canonical transforming growth factor-β signaling by the loss of Smad4 expression in TECs leads to qualitative changes in TEC function and a progressively disorganized thymic microenvironment. Moreover, the number of thymus resident early T-lineage progenitors is severely reduced in the absence of Smad4 expression in TECs and directly correlates with extensive thymic and peripheral lymphopenia. Our observations hence place Smad4 within the signaling events in TECs that determine total thymus cellularity by controlling the number of early T-lineage progenitors.


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