Janus kinase inhibitors alter NK cell phenotypes and inhibit their antitumour capacity
Authors' conclusion
JAKi have a phenotypic and functional impact on NK cell activation and impair their antitumour activity, with a variable impact depending on the JAKi.
Study context
- Population
- RA patients treated with tofacitinib (TOFA), baricitinib (BARI) or MTX; sorted NK cells from healthy donors
- Participants
- 28 RA patients
- Comparison
- Janus kinase inhibitors (JAKi) vs MTX ex vivo and vs dimethyl sulphoxide (DMSO) in vitro
- Outcome
- NK cell phenotype (CD69, CD57, NKp30) and function (CD107a, IFN-γ/TNF, cytotoxicity) under JAKi
Methodological detailsex vivo phenotyping, in vitro, three concentrations including therapeutic concentration
- Ex vivo phenotyping
- In vitro
- Three concentrations including therapeutic concentration
Main finding
As reported in the abstract
- NKp30-stimulated NK cells with TOFA: reduced CD107a
- P < 0.01
- NKp30-stimulated NK cells with TOFA: reduced IFN-γ/TNF expression
- P < 0.05
- NK cells exposed to TOFA co-cultured with A549 and SU-DHL-4: reduced CD107a
- P < 0.05
- NK cells exposed to TOFA co-cultured with A549 and SU-DHL-4: altered cytotoxicity
- P < 0.05
Original publication
Janus kinase inhibitors alter NK cell phenotypes and inhibit their antitumour capacity. Rheumatology (Oxford). Published 30 December 2022. doi:10.
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