The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1996/12/2417/ $5.00
The Journal of Experimental Medicine, Volume 184, Number 6, December 1, 1996 2417-2422

Brief Definitive Reports

A Role for Endogenous Transforming Growth Factor β1 in Langerhans Cell Biology: The Skin of Transforming Growth Factor β1 Null Mice Is Devoid of Epidermal Langerhans Cells

Teresa A. Borkowski*, John J. Letterio{ddagger}, Andrew G. Farr§, and Mark C. Udey*

From the * Dermatology Branch and {ddagger} the Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-1908; and the § Department of Biological Structure, University of Washington, Seattle, Washington 98195

Transforming growth factor β1 (TGF-β1) regulates leukocytes and epithelial cells. To determine whether the pleiotropic effects of TGF-β1, a cytokine that is produced by both keratinocytes and Langerhans cells (LC), extend to epidermal leukocytes, we characterized LC (the epidermal contingent of the dendritic cell [DC] lineage) and dendritic epidermal T cells (DETC) in TGF-β1 null (TGF-β1 –/–) mice. I-A+ LC were not detected in epidermal cell suspensions or epidermal sheets prepared from TGF-β1 –/– mice, and epidermal cell suspensions were devoid of allostimulatory activity. In contrast, TCR-{gamma}{delta}+ DETC were normal in number and appearance in TGF-β1 –/– mice and, importantly, DETC represented the only leukocytes in the epidermis. Immunolocalization studies revealed CD11c+ DC in lymph nodes from TGF-β1 –/– mice, although gp40+ DC were absent. Treatment of TGF-β1 –/– mice with rapamycin abrogated the characteristic inflammatory wasting syndrome and prolonged survival indefinitely, but did not result in population of the epidermis with LC. Thus, the LC abnormality in TGF-β1 –/– mice is not a consequence of inflammation in skin or other organs, and LC development is not simply delayed in these animals. We conclude that endogenous TGF-β1 is essential for normal murine LC development or epidermal localization.

Address correspondence to Dr. Mark C. Udey, Dermatology Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 12N238, Bethesda, MD 20892-1908.


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