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Published 1 March 2004. doi:10.1084/jem.20031973
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 199, Number 5, 607-615
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Pre-TCR{alpha} and TCR{alpha} Are Not Interchangeable Partners of TCRß during T Lymphocyte Development

Christine Borowski, Xiaoyan Li, Iannis Aifantis, Fotini Gounari, and Harald von Boehmer

Department of Pathology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115

Address correspondence to Harald von Boehmer, Dept. of Pathology, Harvard Medical School, Dana-Farber Cancer Institute, Smith Building Room 736, 1 Jimmy Fund Way, Boston, MA 02115. Phone: (617) 632-6880; Fax: (617) 632-6881; email: harald_von_Boehmer{at}dfci.harvard.edu

In contrast with the {alpha}ß T cell receptor (TCR), the pre-TCR spontaneously segregates to membrane rafts from where it signals in a cell-autonomous fashion. The disparate behaviors of these two receptors may stem either from differences inherent to the distinct developmental stages during which they are expressed, or from features intrinsic and unique to the receptor components themselves. Here, we express TCR{alpha} precisely at the pre-TCR checkpoint, at levels resembling those of endogenous pre-TCR{alpha} (pT{alpha}), and in the absence of endogenous pT{alpha}. Both in isolation and more dramatically when in competition with pT{alpha}, TCR{alpha} induced defective proliferation, survival, and differentiation of {alpha}ß T lymphocyte precursors, as well as impaired commitment to the {alpha}ß T lymphocyte lineage. Substitution of TCR{alpha} transmembrane and cytoplasmic domains with those of pT{alpha} generated a hybrid molecule possessing enhanced competitive abilities. We conclude that features intrinsic to the pre-TCR, which are absent in TCR{alpha}, are essential for its unique function.

Key Words: T lymphocyte subsets • cell lineage • receptor-mediated signal transduction • receptor antigen • T-cell {gamma}{delta}

The online version of this article includes supplemental material.

The present address of I. Aifantis is The University of Chicago, Dept. of Medicine, Section of Rheumatology, Chicago, IL 60637.

The present address of F. Gounari is Tufts University, New England Medical Center, Molecular Oncology Research Institute, Boston, MA 02115.

Abbreviations used in this paper: DN, CD4-8- double negative; EGFP, enhanced green fluorescent protein; FTOC, fetal thymic organ culture; HSA, heat-stable antigen; pT{alpha}, pre-TCR{alpha}; WTpT{alpha}, wild-type pT{alpha}.


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