An antibody specific for Tcrb-V10a and Tcrb-V10c

Tomonari, Kyuhei; Rosenwasser, Oliver A.; Fairchild, Susan P.

doi:10.1007/s002510050316

Cited by 2 publications

(1 citation statement)

References 2 publications

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“…The following mAb were used: B20.6 (anti-V g 2); KJ25 (anti-V g 3.1); KJ23 (anti-V g 3.2); KT4-10 (anti-V g 4); MR9-4 (anti-V g 5.1-2); 44.22.1 (anti-V g 6); TR310 (anti-V g 7); F23.2 (anti-V g 8.2); KJ16 (anti-V g 8.1-2); F23.1 (anti-V g 8.1-3); MR10-2 (anti-V g 9); B21.5 (anti-V g 10 b ), KT10a (anti-V g 10 a/c ) [41]; RR3-15 (anti-V g 11); MR11-1 (anti-V g 12); 14.2 (anti-V g 14); FITC-labeled anti-B220 (RA3-3A1), PE-labeled anti-CD4 (H129. 19) and anti-CD8 (53-6.7) (Caltag laboratories, San Francisco, CA).…”

Section: Monoclonal Antibodiesmentioning

confidence: 99%

Differential reactivity of TCR Vβ10 alleles to a mouse mammary tumor virus superantigen

et al. 1998

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Mouse mammary tumor virus (MMTV) expresses a superantigen (SAg) which plays a critical role in the viral life cycle. We have recently described the new infectious MMTV (SIM) encoding a Vbeta4-specific SAg in mice with a TCR-Vbeta(b) haplotype. We have now compared the SAg activity of this virus in BALB/c mice harboring the TCR-Vbeta(a), TCR-Vbeta(b) or TCR-Vbeta(c) haplotypes which differ by a central deletion in the TCR-Vbeta(a) and TCR-Vbeta(c) locus and by mutations in some of the remaining Vbeta elements. Injection of MMTV (SIM) led to a strong stimulation of Vbeta4+ CD4+ T cells in TCR-Vbeta(b) mice, but only to a weak stimulation of these cells in TCR-Vbeta(a) or TCR-Vbeta(c) mice. A large increase in the percentage of Vbeta10+ cells was observed among CD4+ T cells in mice with the Vbeta(a) or Vbeta(c), but not the Vbeta(b) TCR-Vbeta haplotype. Vbeta10+ cells dominated the response when Vbeta10(a/c) and Vbeta4 subsets were present together. This is the first report of a viral SAg interacting with murine Vbeta10+ cells. Six amino acid differences between Vbeta10(a/c) and Vbeta10(b) could account for the gain of reactivity of Vbeta10(a/c) to the MMTV(SIM) SAg. No mutations were found in the hypervariable region 4 (HV4) of the TCR. Mutations at positions 22 and 28 introduce into Vbeta10(a/c) the same amino acids which are found at these positions in the MMTV(SIM)-reactive Vbeta4. Tridimensional models indicated that these amino acids lie close to HV4 and are likely to be important for the interaction of the SAg with the TCR.

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Section: Monoclonal Antibodiesmentioning

confidence: 99%

Differential reactivity of TCR Vβ10 alleles to a mouse mammary tumor virus superantigen

et al. 1998

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Dramatic Influence of Vβ Gene Polymorphism on an Antigen-Specific CD8+ T Cell Response In Vivo

Bour

Michielin²,

Bousso

et al. 1999

The Journal of Immunology

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According to recent crystallographic studies, the TCR-αβ contacts MHC class I-bound antigenic peptides via the polymorphic V gene-encoded complementarity-determining region 1β (CDR1β) and the hypervariable (D)J-encoded CDR3β and CDR3α domains. To evaluate directly the relative importance of CDR1β polymorphism on the fine specificity of T cell responses in vivo, we have taken advantage of congenic Vβa and Vβb mouse strains that differ by a CDR1 polymorphism in the Vβ10 gene segment. The Vβ10-restricted CD8+ T cell response to a defined immunodominant epitope was dramatically reduced in Vβa compared with Vβb mice, as measured either by the expansion of Vβ10+ cells or by the binding of MHC-peptide tetramers. These data indicate that Vβ polymorphism has an important impact on TCR-ligand binding in vivo, presumably by modifying the affinity of CDR1β-peptide interactions.

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An antibody specific for Tcrb-V10a and Tcrb-V10c

Cited by 2 publications

References 2 publications

Differential reactivity of TCR Vβ10 alleles to a mouse mammary tumor virus superantigen

Differential reactivity of TCR Vβ10 alleles to a mouse mammary tumor virus superantigen

Dramatic Influence of Vβ Gene Polymorphism on an Antigen-Specific CD8+ T Cell Response In Vivo

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