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Anti-6-FP T cell receptor (M33.64(Y95F)), pCDTCR1 (TCR-YC0046)


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

The M33.64 cell line was activated in response to 5-OP-RU and E. coli but also exhibited robust, MR1-dependent activation in the absence of added Ag, consistent with it being stained with empty MR1 tetramer. The MAV36 TCR+ cells were activated when co-cultured with C1R.MR1 cells in the presence of E. coli or 5-OP-RU, but showed little response without added Ag. To further investigate the M33.64 TCR autoreactivity, the M33.64 TCR+ cell line was co-cultured with MR1-transduced C1R cells that were flow cytometrically sorted based on graded MR1 expression. The M33.64 TCR+ cells upregulated CD69 in an MR1-dose-dependent manner, without added Ag, confirming that in contrast to other MAIT TCRs, the M33.64 TCR is MR1 autoreactive.

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Details

  • Target
  • 6-FP
  • Epitope
  • 6-formylpterin
  • Format
  • Modified TCR
  • Allele
  • human MR1
  • Vector Name
  • pCDTCR1
  • Vector Length
  • ~ 8 kb
  • Vector Type
  • Lentiviral vector
  • TCR Clone
  • M33.64(Y95F)
  • Host Species
  • Human

Target

  • Introduction
  • The MAIT TCR is restricted by the MHC class I–related molecule MR1. MR1 is a monomorphic Ag-presenting molecule that is highly conserved across mammals. Although the MR1 transcript is expressed widely, cell surface expression of MR1 is very low/absent, thereby indicating that other factors, including Ag supply, can determine the level of MR1 that egresses to the cell membrane. Recently, it has been established that MR1 can bind vitamin B–based precursors and derivatives that originate from folic acid (vitamin B9) and riboflavin (vitamin B2) biosynthesis. Specifically, MR1 can present 6-formylpterin (6-FP), a naturally occurring photo-degradation product of folic acid, and a series of ribityllumazines, including 6,7-dimethyl-8-d-ribityllumazine (RL-6,7-DiMe), 6-methyl-7-hydroxy-8-d-ribityllumazine (RL-6-Me-7-OH), 5-(2-oxoethylideneamino)-6-d-ribitylaminouracil (5-OE-RU), and 5-(2-oxopropylideneamino)-6-d-ribitylaminouracil (5-OP-RU). The MR1 Ag-binding cleft is ideally disposed to bind to these small organic metabolites, with the ligands being closely sequestered by an aromatic cradle within MR1, whereupon some of the ligands can form a covalent bond (Schiff base) with MR1.

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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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