Targeting BTLA with the peptide inhibitor HVEM(14-39) - A new way to restore the activity of T cells in melanoma.
Biomed Pharmacother
; 175: 116675, 2024 Jun.
Article
en En
| MEDLINE
| ID: mdl-38733770
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.
Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Receptores Inmunológicos
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Proliferación Celular
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Miembro 14 de Receptores del Factor de Necrosis Tumoral
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Melanoma
Límite:
Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Biomed Pharmacother
Año:
2024
Tipo del documento:
Article
País de afiliación:
Polonia