PMID- 38162657 OWN - NLM STAT- MEDLINE DCOM- 20240103 LR - 20240401 IS - 1664-3224 (Electronic) IS - 1664-3224 (Linking) VI - 14 DP - 2023 TI - The role of immune checkpoints in antitumor response: a potential antitumor immunotherapy. PG - 1298571 LID - 10.3389/fimmu.2023.1298571 [doi] LID - 1298571 AB - Immunotherapy aims to stimulate the immune system to inhibit tumor growth or prevent metastases. Tumor cells primarily employ altered expression of human leukocyte antigen (HLA) as a mechanism to avoid immune recognition and antitumor immune response. The antitumor immune response is primarily mediated by CD8+ cytotoxic T cells (CTLs) and natural killer (NK) cells, which plays a key role in the overall anti-tumor immune response. It is crucial to comprehend the molecular events occurring during the activation and subsequent regulation of these cell populations. The interaction between antigenic peptides presented on HLA-I molecules and the T-cell receptor (TCR) constitutes the initial signal required for T cell activation. Once activated, in physiologic circumstances, immune checkpoint expression by T cells suppress T cell effector functions when the antigen is removed, to ensures the maintenance of self-tolerance, immune homeostasis, and prevention of autoimmunity. However, in cancer, the overexpression of these molecules represents a common method through which tumor cells evade immune surveillance. Numerous therapeutic antibodies have been developed to inhibit immune checkpoints, demonstrating antitumor activity with fewer side effects compared to traditional chemotherapy. Nevertheless, it's worth noting that many immune checkpoint expressions occur after T cell activation and consequently, altered HLA expression on tumor cells could diminish the clinical efficacy of these antibodies. This review provides an in-depth exploration of immune checkpoint molecules, their corresponding blocking antibodies, and their clinical applications. CI - Copyright (c) 2023 Mejia-Guarnizo, Monroy-Camacho, Turizo-Smith and Rodriguez-Garcia. FAU - Mejia-Guarnizo, Lidy Vannessa AU - Mejia-Guarnizo LV AD - Cancer Biology Research Group, Instituto Nacional de Cancerologia, Bogota, Colombia. AD - Sciences Faculty, Master in Microbiology, Universidad Nacional de Colombia, Bogota, Colombia. FAU - Monroy-Camacho, Paula Stefany AU - Monroy-Camacho PS AD - Cancer Biology Research Group, Instituto Nacional de Cancerologia, Bogota, Colombia. FAU - Turizo-Smith, Andres David AU - Turizo-Smith AD AD - Medicine Faculty, Universidad Nacional de Colombia, Bogota, Colombia. FAU - Rodriguez-Garcia, Josefa Antonia AU - Rodriguez-Garcia JA AD - Cancer Biology Research Group, Instituto Nacional de Cancerologia, Bogota, Colombia. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20231215 PL - Switzerland TA - Front Immunol JT - Frontiers in immunology JID - 101560960 RN - 0 (Antibodies) RN - 0 (Histocompatibility Antigens Class I) RN - 0 (HLA Antigens) SB - IM MH - Humans MH - *Neoplasms MH - T-Lymphocytes, Cytotoxic MH - Immunotherapy/methods MH - Killer Cells, Natural MH - Antibodies MH - Histocompatibility Antigens Class I MH - HLA Antigens PMC - PMC10757365 OTO - NOTNLM OT - HLA antigens OT - immune checkpoint inhibitors OT - immune evasion OT - immunotherapy OT - neoplasms COIS- The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. EDAT- 2024/01/02 11:43 MHDA- 2024/01/03 09:44 PMCR- 2023/01/01 CRDT- 2024/01/01 04:27 PHST- 2023/09/21 00:00 [received] PHST- 2023/11/29 00:00 [accepted] PHST- 2024/01/03 09:44 [medline] PHST- 2024/01/02 11:43 [pubmed] PHST- 2024/01/01 04:27 [entrez] PHST- 2023/01/01 00:00 [pmc-release] AID - 10.3389/fimmu.2023.1298571 [doi] PST - epublish SO - Front Immunol. 2023 Dec 15;14:1298571. doi: 10.3389/fimmu.2023.1298571. eCollection 2023.