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Original Article

Premature Expression of T Cell Receptor (Tcr)β Suppresses Tcr Gene Rearrangement but Permits Development of Lineage T Cells

^a Laboratory of Cellular and Molecular Immunology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0420
Bldg. 4, Rm. 111, Laboratory of Cellular and Molecular Immunology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-0420.301-402-4891301-496-5530

bfowlkes{at}nih.gov

The T cell receptor (TCR) and the pre-TCR promote survival and maturation of early thymocyte precursors. Whether these receptors also influence versus β lineage determination is less clear. We show here that TCR gene rearrangements are suppressed in TCRβ transgenic mice when the TCRβ is expressed early in T cell development. This situation offers the opportunity to examine the outcome of versus β T lineage commitment when only the TCRβ is expressed. We find that precursor thymocytes expressing TCRβ not only mature in the β pathway as expected, but also as CD4^–CD8^– T cells with properties of lineage cells. In TCRβ transgenic mice, in which the transgenic receptor is expressed relatively late, TCR rearrangements occur normally such that TCRβ⁺CD4^–CD8^– cells co-express TCR. The results support the notion that TCRβ can substitute for TCR to permit a lineage choice and maturation in the lineage. The findings could fit a model in which lineage commitment is determined before or independent of TCR gene rearrangement. However, these results could be compatible with a model in which distinct signals bias lineage choice and these signaling differences are not absolute or intrinsic to the specific TCR structure.

Key Words: lineage commitment • TCR transgenic mice • thymus • differentiation • positive selection

Abbreviations used in this paper: APC, allophycocyanin; β₂m, β₂-microglobulin; B6, C57BL/6; B10, C57BL/10; CsA, cyclosporine A; HSA, heat stable antigen; RAG, recombination activating gene; TCRβDN, TCRβ⁺CD4^–CD8^–.

K. Terrence and C.P. Pavlovich contributed equally to this work.

© 2000 The Rockefeller University Press

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