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Id3 Restricts the Developmental Potential of Lineage during Thymopoiesis¹

Ikuko Ueda-Hayakawa^*,, Josh Mahlios^* and Yuan Zhuang^2,*

^* Department of Immunology, Duke University Medical Center, Durham, NC 27710; Department of Dermatology, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa, Japan

Most T cell progenitors develop into the β T cell lineage with the exception of a small fraction contributing to the lineage throughout postnatal life. T cell progenitors usually commit to the β lineage upon the expression of a fully rearranged and functional TCRβ gene, and most cells that fail to produce a functional TCRβ-chain will die instead of adopting the alternative T cell fate. What prevents these cells from continuing TCR rearrangement and adopting the T cell fate is not known. In this study, we show that functional loss of Id3 results in a significant increase of T cell production from progenitor cells undergoing TCRβ rearrangement. The enhanced T cell development correlated with increased TCR gene rearrangement involving primarily V1.1 in Id3 deficient mice. We further show that Id3 deficiency promotes T cell production in a manner independent of TCRβ-chain expression. Our data indicates that Id3 suppresses V1.1 rearrangement and lineage potential among T cell progenitors that have completed TCRβ gene rearrangement without producing a functional TCRβ protein.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work has been supported by National Institute of Health (CA072433, GM059638, and RR024927 to Y.Z.), Arthritis Foundation (to Y.Z.), and the Ministry of Education, Science, and Culture of Japan (to I.U.-H.).

² Address correspondence and reprint requests to Dr. Yuan Zhuang, Department of Immunology, Duke University Medical Center, Box 3010, Durham, NC 27710. E-mail address: yzhuang{at}duke.edu

³ Abbreviations used in this paper: DN, double negative; 7-AAD, 7-aminoactinomycin D; DP, double positive.