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Anti-2.5mi 5G 9D T cell receptor (#61), pCDTCR1 (TCR-YC0013)


All products and services are For Research Use Only and CANNOT be used in the treatment or diagnosis of disease.

It was examined that the BDC 2.5-like T cell response in NOD mice by sorting and analyzing single cells with I-Ag7 tetramers displaying BDC 2.5 peptide mimotopes with either a negative charge (HHPIWARMDA; hereafter referred to as 2.5mi) or no charge at P9 (G or Q, named P9G and P9Q thereafter, HHPIWARMG/QA). The sequencing of individual TCR segments revealed an increase of negative residues in the CDR3β N-terminal region from cells sorted with P9Q or P9G tetramers (16/31, 52%) as compared with cells sorted with P9D tetramers (5/23, 21%). The latter frequency was comparable to the normal frequency of negative charges found in all purified CD4+ CDR3β sequences in NOD mice. The negative charges found in the CDR3β of the P9Q and P9G populations were encoded by N additions or deletions, suggesting an antigen-driven process. This belief was also supported by the fact that P9G or P9Q tetramer–positive cells were found in higher numbers in the periphery than in the thymus and that over time, the population expanded early (3–4 weeks), then contracted (6–12 weeks) to reexpand later, especially in diabetic animals. In addition, the BDC 2.5 9Q/9G reactive TCR populations were found, up until week twelve, to be larger than the corresponding BDC 2.5 9D populations.

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Details

  • Target
  • 2.5mi 5G 9D
  • Epitope
  • AHHPIWARMDA
  • Format
  • Non-Modified TCR
  • Allele
  • H2-IAg7
  • Vector Name
  • pCDTCR1
  • Vector Length
  • ~ 8 kb
  • Vector Type
  • Lentiviral vector
  • TCR Clone
  • #61
  • Host Species
  • Mouse

Target

  • Introduction
  • An association between the HLA locus and autoimmune dysfunction was suggested as early as 1971. Later, attention focused on MHC class II genes with the discovery of an association between HLA-DR4 and rheumatoid arthritis in 1978. Thirty years have now passed since these seminal studies, and yet our general understanding of antigen presentation and T cell recognition at a molecular level has not provided an expected explanation for this association. One of the most striking examples of MHC allele linkage disequilibrium with autoimmune diseases is provided by type I diabetes (T1D) and the identification of a single residue polymorphism that confers either susceptibility or resistance to the disease. Indeed, almost all alleles linked to T1D share a common nonaspartic acid residue at position 57 of their β chain. The absence of a negative charge at β57 eliminates an interdomain salt bridge between Argα76 and β57; however, this substitution does not compromise the overall stability of the molecule or its capacity to bind peptide. The absence of a negative charge at β57 reshapes the P9 pocket of the HLA-DQ8/I-Ag7 peptide-binding groove and exposes a large positively charged patch on the MHC surface. An important functional consequence of this β57 polymorphism is a clear propensity for these MHC molecules to bind peptides with a negatively charged residue at position P9. However, this feature is not absolute and many noncharged P9 peptides efficiently bind diabetogenic MHC molecules, such as HLA-DQ8 or I-Ag7. These peptide-MHC (pMHC) complexes will as a result characteristically have an exposed positive P9 patch on the MHC surface due to the "unpaired" charged Argα76 residue.

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For research use only. Not intended for any clinical use. No products from Creative Biolabs may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative Biolabs.

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