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Targeting BTLA with the peptide inhibitor HVEM(14-39) – A new way to restore the activity of T cells in melanoma.
- Source :
-
Biomedicine & Pharmacotherapy . Jun2024, Vol. 175, pN.PAG-N.PAG. 1p. - Publication Year :
- 2024
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Abstract
- The complex of B- and T-lymphocyte attenuator (BTLA) and herpes virus entry mediator (HVEM) plays a critical role in immune regulation and has emerged as a promising therapeutic target for cancer treatment. In this study, we investigated the potential of the peptide inhibitor HVEM(14-39) to restore peripheral T cell activity in patients with advanced melanoma. In these patients, CD8+ T cells downregulated BTLA expression and increased HVEM expression upon activation. The addition of HVEM(14-39) reduced the percentage of BTLA+ CD8+ T cells and increased the subpopulation of HVEM+ CD8+ T cells. Additionally, HVEM(14-39) enhanced T cell activation, proliferation, and the shift toward effector memory T cell subpopulations. Finally, this peptide affected the proliferation rate and late apoptosis of melanoma cell line in co-culture with T cells. These findings suggest that HVEM(14-39) can overcome T cell exhaustion and improve antitumor responses. Peptide-based immunotherapy targeting the BTLA-HVEM complex offers a promising alternative to monoclonal antibody-based therapies, with the potential for fewer side effects and higher treatment efficacy. [Display omitted] • Targeting the BTLA/HVEM complex improves function of T cells in melanoma patients. • Peptide inhibitor HVEM(14−39) regains T-cell activation potential. • HVEM(14−39) may overcome T-cell exhaustion in cancer patients. • Peptide drugs as a promising solution for cancer immunotherapy. • HVEM(14−39) increases the proliferation of T-cell population in melanoma patients. [ABSTRACT FROM AUTHOR]
- Subjects :
- *T cells
*PEPTIDES
*T-cell exhaustion
*MELANOMA
*IMMUNOLOGIC memory
Subjects
Details
- Language :
- English
- ISSN :
- 07533322
- Volume :
- 175
- Database :
- Academic Search Index
- Journal :
- Biomedicine & Pharmacotherapy
- Publication Type :
- Academic Journal
- Accession number :
- 177514004
- Full Text :
- https://doi.org/10.1016/j.biopha.2024.116675