Literature DB >> 19286348

Analysis of T cell receptor beta chains that combine with dominant conserved TRAV5D-4*04 anti-insulin B:9-23 alpha chains.

Li Zhang1, Jean M Jasinski, Masakazu Kobayashi, Bennett Davenport, Kelly Johnson, Howard Davidson, Maki Nakayama, Kathryn Haskins, George S Eisenbarth.   

Abstract

OBJECTIVE: The objective of this study was to define the spectrum of TCR beta chains permissive for T cells with alpha chains containing the conserved TRAV5D-4*04 sequence to target the insulin B:9-23 peptide, a major epitope for initiation of diabetes in the NOD mouse.
MATERIALS AND METHODS: We produced T cell hybridomas from mice with single T cell receptors (BDC12-4.1 TCR alpha(+)beta(+) double transgenic mice and BDC12-4.4 TCR alpha(+)beta(+) double retrogenic mice) or from mice with only the corresponding alpha chains transgene or retrogene and multiple endogenous TCR beta chains.
RESULTS: Hybridomas with the complete BDC12-4.1 and BDC12-4.4 T cell receptors, despite having markedly different TCR beta chains, responded to similar B:9-23 peptides. Approximately 1% of the hybridomas from mice with the fixed TRAV5D-4*04 alpha chains and multiple endogenous beta chains responded to B:9-23 peptides while the majority of hybridomas with different beta chains did not respond. There was no apparent conservation of TCR beta chain sequences in the responding hybridomas.
CONCLUSIONS: Approximately 1% of hybridomas utilizing different TCR beta chains paired with the conserved TRAV5D-4*04 containing alpha chains respond to insulin peptide B:9-23. Therefore, TCR beta chain sequences make an important contribution to insulin B:9-23 peptide recognition but multiple beta chain sequences are permissive for recognition.

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Year:  2009        PMID: 19286348      PMCID: PMC4383244          DOI: 10.1016/j.jaut.2009.02.003

Source DB:  PubMed          Journal:  J Autoimmun        ISSN: 0896-8411            Impact factor:   7.094


  45 in total

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Review 2.  Extreme genetic risk for type 1A diabetes in the post-genome era.

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4.  Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice.

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5.  Expanded T cells from pancreatic lymph nodes of type 1 diabetic subjects recognize an insulin epitope.

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6.  Autoreactive CD8 T cells associated with beta cell destruction in type 1 diabetes.

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10.  Insulin-induced remission in new-onset NOD mice is maintained by the PD-1-PD-L1 pathway.

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  18 in total

Review 1.  T-cell receptor retrogenic mice: a rapid, flexible alternative to T-cell receptor transgenic mice.

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2.  Structure-based selection of small molecules to alter allele-specific MHC class II antigen presentation.

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Review 3.  Peptide antigens for gamma/delta T cells.

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5.  Monoclonal antibody blocking the recognition of an insulin peptide-MHC complex modulates type 1 diabetes.

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6.  Gamma delta T cell receptors confer autonomous responsiveness to the insulin-peptide B:9-23.

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8.  Banting Lecture 2009: An unfinished journey: molecular pathogenesis to prevention of type 1A diabetes.

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Review 9.  Molecular Interactions Governing Autoantigen Presentation in Type 1 Diabetes.

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Review 10.  Type 1 diabetes: primary antigen/peptide/register/trimolecular complex.

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