| First Author | Ueda-Hayakawa I | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 9 | Pages | 5306-16 |
| PubMed ID | 19380777 | Mgi Jnum | J:147720 |
| Mgi Id | MGI:3842018 | Doi | 10.4049/jimmunol.0804249 |
| Citation | Ueda-Hayakawa I, et al. (2009) Id3 restricts the developmental potential of gammadelta lineage during thymopoiesis. J Immunol 182(9):5306-16 |
| abstractText | Most T cell progenitors develop into the alphabeta T cell lineage with the exception of a small fraction contributing to the gammadelta lineage throughout postnatal life. T cell progenitors usually commit to the alphabeta lineage upon the expression of a fully rearranged and functional TCRbeta gene, and most cells that fail to produce a functional TCRbeta-chain will die instead of adopting the alternative gammadelta T cell fate. What prevents these cells from continuing TCRgamma rearrangement and adopting the gammadelta T cell fate is not known. In this study, we show that functional loss of Id3 results in a significant increase of gammadelta T cell production from progenitor cells undergoing TCRbeta rearrangement. The enhanced gammadelta T cell development correlated with increased TCRgamma gene rearrangement involving primarily Vgamma1.1 in Id3 deficient mice. We further show that Id3 deficiency promotes gammadelta T cell production in a manner independent of TCRbeta-chain expression. Our data indicates that Id3 suppresses Vgamma1.1 rearrangement and gammadelta lineage potential among T cell progenitors that have completed TCRbeta gene rearrangement without producing a functional TCRbeta protein. |
