Immune checkpoint blockade opens a new way to cancer immunotherapy.
B7-H3
CTAL-4
DGK-α
LAG-3
PD-1
Tim-3
antibody
immune checkpoint
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
22
05
2018
accepted:
01
11
2018
pubmed:
5
12
2018
medline:
14
4
2020
entrez:
5
12
2018
Statut:
ppublish
Résumé
Among the main promising systems to triggering therapeutic antitumor immunity is the blockade of immune checkpoints. Immune checkpoint pathways regulate the control and eradication of infections, malignancies, and resistance against a host of autoantigens. Initiation point of the immune response is T cells, which have a critical role in this pathway. As several immune checkpoints are initiated by ligand-receptor interactions, they can be freely blocked by antibodies or modulated by recombinant forms of ligands or receptors. Antibodies against cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) were the first immunotherapeutics that achieved the US Food and Drug Administration approval. Preliminary clinical results with the blockers of additional immune checkpoint proteins, such as programmed cell death protein 1 (PD-1) indicate extensive and different chances to boost antitumor immunity with the objective of conferring permanent clinical effects. This study provides an overview of the immune checkpoint pathways, including CTLA-4, PD-1, lymphocyte activation gene 3, T-cell immunoglobulin and mucin domain 3, B7-H3, and diacylglycerol kinase α and implications of their inhibition in the cancer therapy.
Substances chimiques
Antineoplastic Agents, Immunological
0
Receptors, Immunologic
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
8541-8549Informations de copyright
© 2018 Wiley Periodicals, Inc.