Id3 Restricts the Developmental Potential of γδ Lineage during Thymopoiesis

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Abstract
Most T cell progenitors develop into the αβ T cell lineage with the exception of a small fraction contributing to the γδ lineage throughout postnatal life. T cell progenitors usually commit to the αβ 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 γδ T cell fate. What prevents these cells from continuing TCRγ rearrangement and adopting the γδ T cell fate is not known. In this study, we show that functional loss of Id3 results in a significant increase of γδ T cell production from progenitor cells undergoing TCRβ rearrangement. The enhanced γδ T cell development correlated with increased TCRγ gene rearrangement involving primarily Vγ1.1 in Id3 deficient mice. We further show that Id3 deficiency promotes γδ T cell production in a manner independent of TCRβ-chain expression. Our data indicates that Id3 suppresses Vγ1.1 rearrangement and γδ lineage potential among T cell progenitors that have completed TCRβ gene rearrangement without producing a functional TCRβ protein.