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Anti-UL83 T cell receptor (r6β), pCDTCR1 (TCR-YC1312)

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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-UL83 T cell receptor (TCR) is constructed for the engineering of T cell to target Tegument protein pp65 (CPSQEPMSIYVY) restricted by HLA-B*35:08. The T cells are genetically modified through transduction with a lentiviral vector expressing UL83-specific T cell receptor.

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Details

  • Target
  • UL83
  • Target Species
  • HCMV
  • Epitope
  • CPSQEPMSIYVY
  • Format
  • Non-Modified TCR
  • Allele
  • HLA-B*35:08
  • Vector Name
  • pCDTCR1
  • Vector Length
  • ~ 8 kb
  • Vector Type
  • Lentiviral vector
  • TCR Clone
  • r6β
  • Host Species
  • Human

Target

  • Introduction
  • pp65 is the most abundant tegument protein and the major constituent of extracellular virus particles. However, pp65 is not essential for the production of new infectious virus particles as evidenced in strains that lack the pp65 gene which can still replicate in culture. pp65 is the major tegument protein responsible for modulating/evading the host cell immune response during HCMV infections. pp65 is implicated in counteracting both innate and adaptive immune responses during HCMV infections. pp65's role in immune evasion is largely attributable to its targeting of both humoral and cellular immunity as well as serving as the dominant target antigen of cytotoxic T lymphocytes. It has been demonstrated that pp65 not only prevents immediate-early proteins from being recognized by components of the immune system, but it also inhibits the synthesis of the various components involved in the host cell's immune response. One of the ways in which pp65 counteracts adaptive immunity is through its enzymatic kinase activity. It was shown that pp65 mediates the phosphorylation of viral immediate-early proteins, which blocks their presentation to the major histocompatibility complex class I molecules. The kinase activity of pp65 has also been implicated in causing the degradation of the alpha chain in the major histocompatibility class II cell surface receptor, HLA-DR, via an accumulation of HLA class II molecules in the lysosome. Furthermore, several studies have presented evidence that pp65 is involved in mediating a decrease in the expression of major histocompatibility complex class II molecules. This is significant in that major histocompatibility complex class I and II molecules are responsible for lymphocyte recognition and antigen presentation with class I molecules presenting to cytotoxic T lymphocytes CD8+ and class II molecules to helper T lymphocytes CD4+.

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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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