THE T-cell receptor (TCR) repertoire is selected in the thymus after rearrangement of genes encoding TCR α and β chains1. Selection is based on the recognition by newly emergent T cells of self-ligands associated with molecules of the major histo-compatibility complex: some combinations result in positive selection, others in negative selection. Negative selection, or clonal deletion, is an important mechanism for eliminating autoreactive T cells. A group of self-ligands involved in clonal deletion was identified because they, like exogenous superantigens2, were recognized by almost all T cells expressing particular TCR Vβ genes. Vβ17a T cells are deleted by a tissue-specific ligand3,4; Vβ6, V07, Vβ8.1 and Vβ9 T cells are deleted by the minor lymphocyte-stimulating (Mls) determinant Mls-la (refs 5–8); Vβ3 T cells by Mls-2a and Mls-3a (refs 9,10); Vβ11 T cells11 by ligands encoded by independently segregating genes; and Vβ5 T cells by ligands encoded by two genes12. Chromosome mapping using recombinant inbred strains of mice and classic backcrosses show that Mls-la in DBA/2 mice is encoded on chromosome 1, that one of the two ligand genes for deletion of Vβ5 T cells maps to chromosome 12 (ref. 12) and that a ligand gene for Vβ11 deletion is linked to the CDS locus on chromosome 6 (ref. 11). Here we present evidence from three sets of backcross mice for concordance between Vβ11 deletion ligand genes on chromosomes 6,12 and 14 and endogenous mouse mammary tumour virus integrant (Mtv) genomes. Our results indicate that the Vβ11 deletion ligands are products of Mtv genomes.
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