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 Blood, 15 October 2008, Vol. 112, No. 8, pp. 3255-3263.
Prepublished online as a Blood First Edition Paper on August 11, 2008; DOI 10.1182/blood-2008-04-153627.

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Submitted April 23, 2008
Accepted July 29, 2008

CCL25 increases thymopoiesis following androgen withdrawal

Kirsten M Williams*, Philip J Lucas, Catherine V Bare, Jiun Wang, Yu-Waye Chu, Ezekiel Tayler, Veena Kapoor, and Ronald E Gress

NCI/Experimental Transplantation and Immunology Branch, National Institutes of Health, Bethesda, MD, United States

* Corresponding author; email: williaki{at}mail.nih.gov.

Although studies have demonstrated that androgen withdrawal increases thymic size, molecular mechanisms underlying this expansion remain largely unknown. We show that decreased androgen signaling leads to enhanced immigration of bone marrow T-cell precursors, as manifested by both an early increase of early thymic progenitors (ETP) and improved uptake of adoptively transferred quantified precursors into congenic castrated hosts. We provide evidence that the ETP niche is enhanced after androgen withdrawal by proliferation of UEA+ thymic epithlelial cell (TEC) and increased TEC production of CCL25, a ligand critical for ETP entry. Moreover, the greatest increase in CCL25 production is by UEA+ TEC, linking function of this subset with the increase in ETP immigration. Furthermore, blockade of CCL25 abrogated the effects of castration by impairing ETP entry, retarding immature thymocyte development, limiting increase of thymic size and impairing increase of thymopoiesis. Collectively, these findings describe a cohesive mechanism underlying increased thymic productivity following androgen withdrawal.


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