IFNλ1 is a STING-dependent mediator of DNA damage and induces immune activation in lung cancer
Downregulation of IFNLR1 can be an immune evasion mechanism developed by cancer cells to avoid responding to endogenous type III IFNs. Thus, rescuing IFNLR1 expression in NSCLC in conjunction to chemotherapy may potentially be harnessed to elevate the anti-tumoral responses.
Authors
- Tina Vilsbøll (ORCID: https://orcid.org/0000-0002-0456-6787)
- Stine Høvring Godsk
- Martin R. Jakobsen (ORCID: https://orcid.org/0000-0001-8847-9201)
- Johanne Ahrenfeldt (ORCID: https://orcid.org/0000-0001-9175-0373)
- Christina T. Jensen
- Kristine Raaby Gammelgaard
Institutions
- Aarhus University (DK)
- Aarhus University Hospital (DK)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2025-02-12
- DOI
- https://doi.org/10.3389/fimmu.2024.1525083
- Citations
- 1
- Primary Topic
- interferon and immune responses
- Type
- article
- Field-Weighted Citation Impact
- 0.80
Funders
- Arvid Nilssons Fond
- Aarhus Universitet
- Kræftens Bekæmpelse
- Lundbeckfonden
- Novo Nordisk
- Dansk Kræftforsknings Fond
- Novo Nordisk Fonden
- Danmarks Frie Forskningsfond
- H. Lundbeck A/S