Leveraging STING, Batf3 Dendritic Cells, CXCR3 Ligands, and Other Components Related to Innate Immunity to Induce a “Hot” Tumor Microenvironment That Is Responsive to Immunotherapy
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In a T-cell-inflamed phenotype, tumor eradication works best and is potentiated by immunotherapy such as checkpoint blockade. However, a majority of patients die despite receiving immunotherapy. One reason is insufficient T cell priming and infiltration in the tumor. Nature provides us with innate immune mechanisms in T-cell-inflamed tumors that we can adopt for more personalized immunotherapy strategies. Tumor sensing through innate signaling pathways and efficient antigen-presenting possess a significant role in bridging innate and adaptive immunity and generating a T-cell-inflamed tumor. One approach to strengthen these innate immune mechanisms is to deliver innate immune factors such as STING or activated DCs into the tumor microenvironment, in particular in patients resistant to checkpoint blockade. The low number of DCs in the tumor bed could potentially be increased with the growth factor FMS-like tyrosine kinase 3 ligand (Flt3L). CD103+ DCs are integral for three phases of anti-tumor immunity: priming, recruiting, and re-invigoration of effector T cells. Re-activation of dysfunctional T cells is achieved via co-stimulatory molecules such as the 4-1BB ligand. The presence of myeloid-cell-derived CXCL9 and CXCL10 in the tumor microenvironment can predict response to immunotherapy. We outline recent preclinical and clinical approaches to deliver these crucial components bridging innate and adaptive immunity into the tumor microenvironment.
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CD8+IFN-γ+ T cells are an effector population shown to be a target of downstream STING signaling involving the IFN-β-CXCL9/10 axis.
“an effector population shown to be a target of downstream STING signaling involving the IFN-β-CXCL9/10 axis.54–58”
From Functional tumor cell-intrinsic STING, not host STING, drives local and systemic antitumor immunity and therapy efficacy following cryoablation (2023) · cites this paper as [58]
Section 3.1 (page unavailable) states that STING-induced CXCL9/10 expression depends on type I interferons, including IFN-β. Section 3 (page unavailable) says CXCL9/10 promote T-cell migration and are associated with CD8+ effector T cells. The paper does not specifically identify CD8+IFN-γ+ T cells as a demonstrated target of that signaling axis. (LLM, conf=0.85)
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Innate Immunity and Tertiary Lymphoid Structures
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- Authors
- Reschke, R., & Olson, D.
- Affiliations
- University of Chicago (US)
- Corresponding author
- Reschke, Robin
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2022-05-16
- Volume
- 14
- Issue
- 10
- Pages
- 2458
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC9139434
- OpenAlex
- W4280530848
- Cited by
- 28
- References
- 75
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 9 · 2023: 7 · 2022: 1
- FWCI
- 0.58
- Type
- journal article
- Language
- en
- Update notices
- correction (2022-05-16)
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- German Research foundation (DFG RE 4468/1-1)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- STING, CXCR3 ligands, CXCL9, CXCL10, Flt3L, tumor microenvironment, immune checkpoint blockade, immunotherapy resistance, innate immunity, antigen presentation, CD103+ dendritic cells, T cell priming, tumor-infiltrating T cells, adoptive immunotherapy
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