Id3 restricts the developmental potential of gamma delta lineage during thymopoiesis.
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.
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Related Subject Headings
- Thymus Gland
- Receptors, Antigen, T-Cell, gamma-delta
- Mice, Mutant Strains
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Inhibitor of Differentiation Proteins
- Immunology
- Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor
- Gene Rearrangement, delta-Chain T-Cell Antigen Receptor
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Thymus Gland
- Receptors, Antigen, T-Cell, gamma-delta
- Mice, Mutant Strains
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Inhibitor of Differentiation Proteins
- Immunology
- Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor
- Gene Rearrangement, delta-Chain T-Cell Antigen Receptor