GM-CSF: Master regulator of the T cell-phagocyte interface during inflammation
Open accessAbstract
The role of granulocyte-macrophage colony-stimulating factor (GM-CSF) was sequentially redefined during the past decades. Originally described as a hematopoietic growth factor for myelopoiesis, GM-CSF was recognized as a central mediator of inflammation bridging the innate and adaptive arms of the immune system. Phagocytes sensing GM-CSF adapt an inflammatory phenotype and facilitate pathogen clearance. However, in the context of chronic tissue inflammation, GM-CSF secreted by tissue-invading lymphocytes has detrimental effects by licensing tissue damage and hyperinflammation. Accordingly, therapeutic intervention at the T cell-phagocyte interface represents an attractive target to ameliorate disease progression and immunopathology. Although GM-CSF is largely dispensable for steady state myelopoiesis, dysregulation, as seen in chronic inflammatory diseases, may however lead to disrupted haematopoiesis and long-term effects on bone marrow output. Here, we will survey the role of GM-CSF during inflammation, discuss the extent to which GM-CSF-secreting T cells, debate their introduction as a separate T cell lineage and explore current and future clinical implications of GM-CSF in human disease settings.
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In the Il10−/− model of colitis, Th17 cells are the main immune population mediating the inflammatory response.
“In the Il10−/− model of colitis, in which IL-10-deficient mice develop spontaneous microbiota-dependent colitis, Th17 cells were identified as the main immune population mediating the inflammatory immune response [43, 133].”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [133]
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Cited by
Sorted by citations
TH17 cell heterogeneity and its role in tissue inflammation
Schnell, A., Littman, D. R., & Kuchroo, V. K. (2023) · Nature Immunology · doi:10.1038/s41590-022-01387-9 · Cited by 286 · see citing works
- Authors
- Ingelfinger, F., De Feo, D., & Becher, B.
- Affiliations
- University of Zurich (CH)
- Corresponding author
- Becher, Burkhard
- Venue
- Seminars in Immunology
- Publisher
- Elsevier BV
- Published
- 2021-04
- Volume
- 54
- Pages
- 101518
- ISSN
- 1044-5323 (ISSN-L)
- OpenAlex
- W3214090945
- Cited by
- 61
- References
- 168
- Citations by year
- 2026: 13 · 2025: 10 · 2024: 12 · 2023: 11 · 2022: 15
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Seminars in Immunology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by-nc-nd)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by-nc-nd)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Universität Zürich (K-41302-10-01)
- Horizon 2020 Framework Programme (826121, 847782, 882424)
- Schweizerische Multiple Sklerose Gesellschaft
- European Research Council
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Studienstiftung des Deutschen Volkes
- Israel Ports Company
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- GM-CSF, inflammation, myelopoiesis, phagocyte activation, hyperinflammation, tissue damage, T cell lineage, hematopoiesis, innate-adaptive immune crosstalk, immunopathology, GM-CSF therapy
- MeSH terms
- Hematopoiesis, Humans, Inflammation, Phagocytes, T-Lymphocytes, Granulocyte-Macrophage Colony-Stimulating Factor
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