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© The Rockefeller University Press, 0022-1007/1997/2/499/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 3, February 3, 1997 499-506

Articles

Abnormal Development of Intestinal Intraepithelial Lymphocytes and Peripheral Natural Killer Cells in Mice Lacking the IL-2 Receptor β Chain

Haruhiko Suzuki{ddagger},§, Gordon S. Duncan*, Hiroaki Takimoto{ddagger},§, and Tak W. Mak*,{ddagger},§

From the * Amgen Institute, {ddagger} Ontario Cancer Institute, and § Departments of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario, Canada M5G 2C1

The interleukin-2 receptor β chain (IL-2Rβ) is expressed on a variety of hematopoietic cell types, including natural killer (NK) cells and nonconventional T lymphocyte subsets such as intestinal intraepithelial lymphocytes (IEL). However, the importance of IL-2Rβ-mediated signaling in the growth and development of these cells has yet to be clearly established. We have investigated IEL and NK cells in mice deficient for IL-2Rβ and describe here striking defects in the development of these cells. IL-2Rβ–/– mice exhibited an abnormal IEL cell population, characterized by a dramatic reduction in T cell receptor {alpha}β CD8{alpha}{alpha} and T cell receptor {gamma}{delta} lymphocytes. This selective decrease indicates that IEL can be classified into those whose development and/or differentiation is dependent on IL-2Rβ function and those for which IL-2Rβ–mediated signaling is not essential. NK cell development was also found to be disrupted in IL-2Rβ–deficient mice, characterized by a reduction in NK1.1+CD3– cells in the peripheral circulation and an absence of NK cytotoxic activity in vitro. The dependence of NK cells and certain subclasses of IEL cells on IL-2Rβ expression points to an essential role for signaling through this receptor, presumably by IL-2 and/or IL-15, in the development of lymphocyte subsets of extrathymic origin.

Address correspondence to Dr. Tak W. Mak, Amgen Institute, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1. H. Suzuki's present address is Department of Immunology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 464, Japan. H. Takimoto's present address is Department of Immunology, Medical Institute of Bioregulation, Kyushu University 69, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812, Japan.

H. Suzuki was supported by a post doctoral fellowship from the Cancer Research Institute, and T.W. Mak by the Medical Research Council of Canada.

The first two authors contributed equally to this study.

1 Abbreviations used in this paper: CM, complete medium; IEL, intraepithelial cells; MNC, mononulear cells; PB, peripheral blood.


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