A cytokine-mediated link between innate immunity, inflammation, and cancer
Open accessAbstract
It has been established that cancer can be promoted and/or exacerbated by inflammation and infections. Indeed, chronic inflammation orchestrates a tumor-supporting microenvironment that is an indispensable participant in the neoplastic process. The mechanisms that link infection, innate immunity, inflammation, and cancer are being unraveled at a fast pace. Important components in this linkage are the cytokines produced by activated innate immune cells that stimulate tumor growth and progression. In addition, soluble mediators produced by cancer cells recruit and activate inflammatory cells, which further stimulate tumor progression. However, inflammatory cells also produce cytokines that can limit tumor growth. Here we provide an overview of the current understanding of the role of inflammation-induced cytokines in tumor initiation, promotion, and progression.
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After chronic stress breaks the balance through a long-term pro-inflammatory response, pro-tumorigenic immune cells and cytokines act on all stages of tumor development including initiation, promotion, malignant transformation, invasion, and metastasis through mutation, epigenetic modification, and regulation of the tumor microenvironment.
“After chronic stress breaks this balance through a long-term pro-inflammatory response, these cells and cytokines can act on all stages of tumor development, including initiation, promotion, malignant transformation, invasion, and metastasis through mutation, epigenetic modification, and regulation of the tumor microenvironment [(50, 51); Figure 3].”
From Chronic Stress Promotes Cancer Development (2020) · cites this paper as [51]
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Immunity, Inflammation, and Cancer
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- Authors
- Lin, W.-W., & Karin, M.
- Affiliations
- National Taiwan University (TW)
- University of California San Diego (US)
- Corresponding author
- Karin, Michael
- Venue
- Journal of Clinical Investigation
- Published
- 2007-05-01
- Volume
- 117
- Issue
- 5
- Pages
- 1175-1183
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1857251
- OpenAlex
- W2133439754
- Cited by
- 1,940
- References
- 128
- Citations by year
- 2026: 18 · 2025: 39 · 2024: 60 · 2023: 92 · 2022: 93 · 2021: 117 · 2020: 117 · 2019: 102 · 2018: 93 · 2017: 123 · 2016: 104 · 2015: 127 · 2014: 134 · 2013: 130 · 2012: 124
- FWCI
- 8.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- cytokines, innate immunity, inflammation, cancer, chronic inflammation, tumor microenvironment, tumor promotion, tumor progression, infection and cancer, tumor initiation, inflammatory cells
- MeSH terms
- Animals, Humans, Immunity, Innate, Inflammation, Neoplasms, Cytokines
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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