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Androgens Accelerate Thymocyte Apoptosis¹

Division of Rheumatology (N.J.O., J.F.) and Endocrinology (S.M.V., W.J.K.), Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Department of Veterans Affairs Medical Center (W.J.K.), Nashville, Tennessee 37212

Address all correspondence and requests for reprints to: Nancy J. Olsen, M.D., T-3219 Medical Center North, Vanderbilt University Medical Center, Nashville Tennessee 37232. E-mail: nancy.j.olsen.2{at}vanderbilt.edu

Mechanisms of androgen-induced thymic involution are largely undefined. We have found that significant decreases in thymic size occur 2–4 h after a dose of testosterone is administered to castrated male mice. This rapid rate of change suggests a role for androgen-induced apoptosis in modulating the size and composition of the thymus. Using thymic organ cultures to define these effects of androgens, we found that dihydrotestosterone treatment of thymus tissues from females or from castrated males results in enhancement of thymocyte apoptosis. Intact (androgen-replete) or testicular feminization, Tfm/Y (androgen-resistant) mice failed to show apoptotic change with androgen treatment, although the apoptotic response to glucocorticoids was present, suggesting a requirement for a functional androgen receptor. Acceleration of thymocyte apoptosis by androgens may mediate processes of thymocyte selection, with the potential to impart gender-specific characteristics on the peripheral T cell repertoire.

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