Journal Article

DKFZ-2022-01119

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png NKG2C+ NK Cells for Immunotherapy of Glioblastoma Multiforme.

Murad, S. ; Michen, S. ; Becker, A. ; Füssel, M. ; Schackert, G. ; Tonn, T. ; Momburg, F.DKFZ* ; Temme, A.

2022
Molecular Diversity Preservation International Basel

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Please use a persistent id in citations: doi:10.3390/ijms23105857

Abstract: In glioblastoma, non-classical human leucocyte antigen E (HLA-E) and HLA-G are frequently overexpressed. HLA-E loaded with peptides derived from HLA class I and from HLA-G contributes to inhibition of natural killer (NK) cells with expression of the inhibitory receptor CD94/NKG2A. We investigated whether NK cells expressing the activating CD94/NKG2C receptor counterpart were able to exert anti-glioma effects. NKG2C+ subsets were preferentially expanded by a feeder cell line engineered to express an artificial disulfide-stabilized trimeric HLA-E ligand (HLA-E*spG). NK cells expanded by a feeder cell line, which facilitates outgrowth of conventional NKG2A+, and fresh NK cells, were included for comparison. Expansion via the HLA-E*spG feeder cells selectively increased the fraction of NKG2C+ NK cells, which displayed a higher frequency of KIR2DL2/L3/S2 and CD16 when compared to expanded NKG2A+ NK cells. NKG2C+ NK cells exhibited increased cytotoxicity against K562 and KIR:HLA-matched and -mismatched primary glioblastoma multiforme (GBM) cells when compared to NKG2A+ NK cells and corresponding fresh NK cells. Cytotoxic responses of NKG2C+ NK cells were even more pronounced when utilizing target cells engineered with HLA-E*spG. These findings support the notion that NKG2C+ NK cells have potential therapeutic value for treating gliomas.

Keyword(s): HLA-E ; HLA-G ; NK cells ; brain cancer ; glioblastoma ; immunotherapy

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Contributing Institute(s):

1. D121 AG Antigenpräsentation und T/NK-Zell-Aktivierung (D121)
2. D120 Angewandte Tumor-Immunität (D120)

Research Program(s):

1. 314 - Immunologie und Krebs (POF4-314) (POF4-314)

Appears in the scientific report 2022

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