The Journal of Experimental Medicine
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Published online 3 April 2000.
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© The Rockefeller University Press, 0022-1007/2000/4/1187/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 7, April 3, 2000 1187-1196

Original Article

Disruption of T Cell Homeostasis in Mice Expressing a T Cell–Specific Dominant Negative Transforming Growth Factor β II Receptor

Philip J. Lucasa, Seong-Jin Kimb, Spencer J. Melbya, and Ronald E. Gressa

a Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892
b Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892
National Institutes of Health, 10 Center Dr. 10/4B-36, Bethesda, MD 20892.301-496-0887301-496-6898

gressr{at}exchange.nih.gov

The immune system, despite its complexity, is maintained at a relative steady state. Mechanisms involved in maintaining lymphocyte homeostasis are poorly understood; however, recent availability of transgenic (Tg) and knockout mouse models with altered balance of lymphocyte cell populations suggest that cytokines play a major role in maintaining lymphocyte homeostasis. We show here that transforming growth factor (TGF)-β plays a critical role in maintaining CD8+ T cell homeostasis in a Tg mouse model that specifically overexpresses a dominant negative TGF-β II receptor (DNRII) on T cells. DNRII T cell Tg mice develop a CD8+ T cell lymphoproliferative disorder resulting in the massive expansion of the lymphoid organs. These CD8+ T cells are phenotypically "naive" except for the upregulation of the cell surface molecule CD44, a molecule usually associated with memory T cells. Despite their dominance in the peripheral lymphoid organs, CD8+ T cells appear to develop normally in the thymus, suggesting that TGF-β exerts its homeostatic control in the peripheral immune system.

Key Words: lymphoproliferative disorder • T lymphocyte subsets • TCR repertoire • T cell transformation • thymocyte development

Abbreviations used in this paper: CCM, complete culture medium; DNRII, dominant negative TGF-β type II receptor; FM, FACS media; HA, hemagglutinin; KO, knockout; RT, reverse transcriptase; Tg, transgenic.

© 2000 The Rockefeller University Press


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