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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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IMMUNOBIOLOGY

CCL25 increases thymopoiesis after androgen withdrawal

Kirsten M. Williams1, Philip J. Lucas1, Catherine V. Bare1, Jiun Wang1, Yu-Waye Chu1, Ezekiel Tayler1, Veena Kapoor1, and Ronald E. Gress1

1 Experimental Transplantation and Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD

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 epithelial cells (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. Taken together, these findings describe a cohesive mechanism underlying increased thymic productivity after androgen withdrawal.


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