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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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V beta 17 gene polymorphism in wild-derived mouse strains: two amino acid substitutions in the V beta 17 region greatly alter T cell receptor specificity.

Of 41 wild-derived mouse strains analyzed, 14 contained T cells bearing V beta 17 receptors in spite of the concomitant expression of I-E antigens. Reciprocal F1 and F2 hybrids of one of these strains, PWK, with laboratory strains revealed different patterns of V beta 17 T cell deletions from those observed with V beta 17 T cells from SJL, implying that the two V beta 17 regions are associated with recognition of distinct superantigens. The structures of the V beta 17 alleles differ by two amino acid substitutions, which lie together in an area distant from the predicted site of T cell receptor interaction with peptide-MHC complexes but overlapping with that implicated in V beta 8.2 recognition of Mls-1 superantigen. This demonstrates that the self-superantigen leading to V beta 17 T cell deletion varies with the allele of the receptor gene and confirms that T cell deletions by such ligands involve interactions with a region of the V beta domain that is distinct from the conventional combining site.[1]

References

  1. V beta 17 gene polymorphism in wild-derived mouse strains: two amino acid substitutions in the V beta 17 region greatly alter T cell receptor specificity. Cazenave, P.A., Marche, P.N., Jouvin-Marche, E., Voegtlé, D., Bonhomme, F., Bandeira, A., Coutinho, A. Cell (1990) [Pubmed]
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