Expression level of BTN3A1 on the surface of CD14
Adult
Aged
Antigens, CD
/ genetics
Butyrophilins
/ genetics
Cell Membrane
/ drug effects
Cell Proliferation
/ drug effects
Female
Gene Expression Regulation
/ drug effects
Humans
Interleukin-2 Receptor alpha Subunit
/ metabolism
Lipopolysaccharide Receptors
/ metabolism
Male
Middle Aged
Monocytes
/ drug effects
Receptors, Antigen, T-Cell, gamma-delta
/ metabolism
Receptors, Fc
/ metabolism
Zoledronic Acid
/ pharmacology
BTN3A1
Monocytes
Vγ9Vδ2 T cells
γδ T cells
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
15 01 2022
15 01 2022
Historique:
received:
07
11
2021
accepted:
16
12
2021
pubmed:
25
12
2021
medline:
9
2
2022
entrez:
24
12
2021
Statut:
ppublish
Résumé
Human γδ T cells expressing Vγ9Vδ2 T cell receptors exert a robust response to pathogens and malignant cells. These cells are activated by BTN3A1, which is expressed by pathogen-derived phosphoantigens (pAgs) or host-derived pAgs that accumulate in transformed cells or in cells exposed to aminobisphosphonates. Activated Vδ2 (+) T cells exert multiple effector functions; therefore, they are a promising candidate for immunotherapy. However, not all donors have γδ T cells with adequate proliferative activity. Here, we performed ex vivo culture of γδ T cells from 20 healthy donors and explored factors that may affect their expansion efficiency. Consistent with previous studies, we found that amplification of γδ T cells requires CD14
Identifiants
pubmed: 34952469
pii: S0006-291X(21)01695-8
doi: 10.1016/j.bbrc.2021.12.060
pii:
doi:
Substances chimiques
Antigens, CD
0
BTN3A1 protein, human
0
Butyrophilins
0
CD14 protein, human
0
Interleukin-2 Receptor alpha Subunit
0
Lipopolysaccharide Receptors
0
Receptors, Antigen, T-Cell, gamma-delta
0
Receptors, Fc
0
Zoledronic Acid
6XC1PAD3KF
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
47-54Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.