TRP2 Peptide (SVYDFFVWL), is an immunopotientor for Melanoma, Neoplasms and Glioma.
This peptide is derived from tyrosinase-related protein 2 (TRP2) residues 180-188. TRP-2 peptide, also named L-dopachrome tautomerase, H-2KB or DCT, belongs to the melanocyte differentiation antigens and has been implicated as a target for immunotherapy of human as well as murine melanoma. Studies show that this TRP2 derived peptide can bind to mouse and human MHC class molecules. Immunization with TRP2 peptide loaded dendritic cells (DCs) results in effective induction of antitumor immunity
SB-PEPTIDE offers to synthesize your peptide in a high purity level for your experiments.
BACKGROUND: Previously we have shown cationic lipid (R)-DOTAP as the immunologically active enantiomer of the DOTAP racemic mixture, initiating complete tumor regression in an exogenous antigen model (murine cervical cancer model). Here, we investigate the use of (R)-DOTAP as an efficacious adjuvant delivering an endogenous antigen in an aggressive murine solid tumor melanoma model.
OBJECTIVE: Showing the ability for Trp2 peptide to break tolerance in peptide vaccine melanoma studies.
METHOD/RESULTS: (R)-DOTAP/Trp2 peptide complexes showed decreasing size and charge with increasing peptide concentration, taking a rod-shape at highest concentrations. The particles were stable for at 2 weeks at 4°C. A dose of 75nmol Trp2 (formulated in (R)-DOTAP) was able to show statistically significant tumor growth delay compared to lower doses of 5 and 25nmol which were no different than untreated tumors. (R)-DOTAP/Trp2 (75nmol) treated mice also showed increased T cell IFN-γ secretion after restimulation with Trp2, as well as CTL activity in vivo. This vaccination group also showed the highest population of functionally active tumor-infiltrating lymphocytes, indicated by IFN-γ secretion after restimulation with Trp2.
CONCLUSION: Thus, (R)-DOTAP has shown the ability to break tolerance as an adjuvant. Its activity to enhance immunogenicity of other tumor associated antigens should be studied further.
BACKGROUND: The induction of a potent and specific T cell response is a major challenge in the development of efficacious cancer vaccine strategies.
OBJECTIVE: Showing that vaccination with liposome-encapsulated TRP2 peptide allows for the stimulation of immune system.
METHOD/RESULTS: We applied a novel liposomal formulation (AVE3) for efficient delivery of antigenic peptides into APCs of the skin. These liposomes resulted in a long-lasting deposition of encapsulated compounds at the injection site and the draining lymph nodes. Using a peptide from the melanocyte differentiation antigen tyrosinase-related protein (TRP2) 2 we could show that vaccination with liposome-encapsulated peptide in combination with oligodeoxynucleotides containing unmethylated CpG motifs (CpG ODNs) as adjuvant leads to the induction of tumor cell-specific cytotoxic T cells. The most potent immune response was observed when both, TRP2 peptide and CpG ODNs, were encapsulated into AVE3. Importantly, in contrast to vaccination with free TRP2 liposomal TRP2 peptide generated T cells which respond to 1000-fold lower antigen concentration. Using the poorly immunogenic B16 melanoma model we could demonstrate that vaccination with liposomal TRP2 peptide plus CpG ODNs but not vaccination with free peptide or adjuvant alone resulted in tumor protection in subcutaneous and metastatic tumor models.
CONCLUSION: In summary, vaccination with liposome-encapsulated peptide antigen and CpG ODN allows for the in vivo loading and activation of DC, thereby generating reactive CTL populations even against poorly immunogenic self-peptide presenting tumors resulting in a potent anti-tumor immune response.
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