Abstract
AbstractThe vast diversity of mammalian adaptive antigen receptors allows for robust and efficient immune responses against a wide number of pathogens. The antigen receptor repertoire is built during the recombination and hypermutation of B and T cell receptor (BCR, TCR) loci. V(D)J recombination rearranges these antigen receptor loci, which are organized as an array of separate V, (D), and J gene segments. Transcription activation at the recombining locus leads to changes in the local three-dimensional architecture, which subsequently contributes to which gene segments are utilized for recombination. The endogenous retrovirus (ERV) mouse mammary tumor provirus 8 (Mtv8) resides on mouse chromosome 6 interposed within the large array of light chain kappa V gene segments. As ERVs contribute to changes in genomic architecture by driving high levels of transcription of neighboring genes, it was suggested thatMtv8could influence the BCR repertoire. We generatedMtv8-deficient mice to determine if the ERV influences V(D)J recombination to test this possibility. We find thatMtv8does not influence the BCR repertoire.
Publisher
Cold Spring Harbor Laboratory