LIR-1 educates expanded human NK cells and defines a unique antitumor NK cell subset with potent antibody-dependent cellular cytotoxicity.
LIR‐1
NK cell education
NK cells
antibody‐dependent cellular cytotoxicity
cancer immunotherapy
Journal
Clinical & translational immunology
ISSN: 2050-0068
Titre abrégé: Clin Transl Immunology
Pays: Australia
ID NLM: 101638268
Informations de publication
Date de publication:
2021
2021
Historique:
received:
08
12
2020
revised:
01
09
2021
accepted:
16
09
2021
entrez:
11
10
2021
pubmed:
12
10
2021
medline:
12
10
2021
Statut:
epublish
Résumé
KIR and NKG2A receptors educate human NK cells to stay responsive to cells with diminished HLA class I. Here, we addressed whether the HLA class I-binding receptor LIR-1 (LILRB1/ILT2/CD85j), which is widely expressed on human NK cells, can mediate education and contribute to antitumor functions of NK cells. Healthy donor NK cells either unstimulated, overnight cytokine-activated or We found that the inhibitory receptor LIR-1 can mediate NK cell education under specific conditions. This novel finding was exclusive to expanded NK cells and further characterisation of the cells revealed high expression of granzyme B and DNAM-1, which both previously have been linked to NK cell education. Corroborating the rheostat education model, LIR-1 co-expression with an educating KIR further increased the responsiveness of expanded NK cells. Inversely, antibody masking of LIR-1 decreased the responsiveness. LIR-1 These findings identify a unique NK cell subset attractive for adoptive cell therapy to treat cancer. Given that LIR-1 binds most HLA class I molecules, this subset may be explored in both autologous and allogeneic settings to innately reject HLA class I
Identifiants
pubmed: 34631057
doi: 10.1002/cti2.1346
pii: CTI21346
pmc: PMC8491220
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e1346Informations de copyright
© 2021 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australian and New Zealand Society for Immunology, Inc.
Déclaration de conflit d'intérêts
The authors declare no competing interest related to this work.
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