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 Blood, 15 October 2006, Vol. 108, No. 8, pp. 2789-2795.
Prepublished online as a Blood First Edition Paper on June 20, 2006; DOI 10.1182/blood-2006-05-025676.

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NEOPLASIA

Dysregulation of IL-15-mediated T-cell homeostasis in TGF-beta dominant-negative receptor transgenic mice

Philip J. Lucas, Seong-Jin Kim, Crystal L. Mackall, William G. Telford, Yu-Waye Chu, Frances T. Hakim, and Ronald E. Gress

From the Experimental Transplantation and Immunology Branch, the Laboratory of Cell Regulation and Carcinogenesis, and the Pediatric Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.

T-cell subpopulations, defined by their expression of CD4, CD8, naive, and memory cell-surface markers, occupy distinct homeostatic compartments that are regulated primarily by cytokines. CD8+ memory T cells, as defined by CD44hi surface expression, are dependent on IL-15 as a positive regulator of their homeostatic maintenance. Manipulation of IL-15 signaling through gene aberration, overexpression, or receptor alterations has been shown to dramatically affect T-cell homeostasis, with overexpression leading to fatal leukemia. Here we show that TGF-beta is the critical negative regulator of murine CD8+ memory T-cell homeostasis with direct opposition to the positive effects of IL-15. This negative regulation is mediated, at least in part, by the ability of TGF-beta to modulate expression of the beta-chain of the IL-15 receptor, thus establishing a central axis between these 2 cytokines for homeostatic control of CD8+ memory T-cell populations. These data establish TGF-beta as a critical and dominant tumor-suppressor pathway opposing IL-15-mediated CD8+ T-cell expansion and potential malignant transformation.


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