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Anti-3-F-SA T cell receptor (A-F7), pCDTCR1 (TCR-YC0037)

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

The vector of anti-3-F-SA T cell receptor (TCR) is constructed for the engineering of T cell to target 3-F-SA (3-formylsalicylic acid) restricted by human MR1. The T cells are genetically modified through transduction with a lentiviral vector expressing 3-F-SA-specific T cell receptor.

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Details

  • Target
  • 3-F-SA
  • Epitope
  • 3-formylsalicylic acid
  • Format
  • Non-Modified TCR
  • Allele
  • human MR1
  • Vector Name
  • pCDTCR1
  • Vector Length
  • ~ 8 kb
  • Vector Type
  • Lentiviral vector
  • TCR Clone
  • A-F7
  • Host Species
  • Human

Target

  • Introduction
  • The major-histocompatibility-complex-(MHC)-class-I-related molecule MR1 can present activating and non-activating vitamin-B-based ligands to mucosal-associated invariant T cells (MAIT cells). Whether MR1 binds other ligands is unknown. Here we identified a range of small organic molecules, drugs, drug metabolites and drug-like molecules, including salicylates and diclofenac, as MR1-binding ligands. Some of these ligands inhibited MAIT cells ex vivo and in vivo, while others, including diclofenac metabolites, were agonists. Crystal structures of a T cell antigen receptor (TCR) from a MAIT cell in complex with MR1 bound to the non-stimulatory and stimulatory compounds showed distinct ligand orientations and contacts within MR1, which highlighted the versatility of the MR1 binding pocket. The findings demonstrated that MR1 was able to capture chemically diverse structures, spanning mono- and bicyclic compounds, that either inhibited or activated MAIT cells. This indicated that drugs and drug-like molecules can modulate MAIT cell function in mammals.

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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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