Secreted Thrombospondin-1 Regulates Macrophage Interleukin-1β Production and Activation through CD47
Open accessAbstract
Thrombospondin-1 regulates inflammation by engaging several cell surface receptors and by modulating activities of other secreted factors. We have uncovered a novel role of thrombospondin-1 in modulating production and activation of the proinflammatory cytokine IL-1β by human and murine macrophages. Physiological concentrations of thrombospondin-1 limit the induction by lipopolysaccharide of IL-1β mRNA and total protein production by human macrophages. This inhibition can be explained by the ability of thrombospondin-1 to disrupt the interaction between CD47 and CD14, thereby limiting activation of NFκB/AP-1 by lipopolysaccharide. Only the CD47-binding domain of thrombospondin-1 exhibits this activity. In contrast, CD47, CD36 and integrin-binding domains of thrombospondin-1 independently enhance the inflammasome-dependent maturation of IL-1β in human THP-1 monocyte-derived macrophages. Correspondingly, mouse bone marrow-derived macrophages that lack either thrombospondin-1 or CD47 exhibit diminished induction of mature IL-1β in response to lipopolysaccharide. Lack of CD47 also limits lipopolysaccharide induction of IL-1β, NLRP3 and caspase-1 mRNAs. These data demonstrate that thrombospondin-1 exerts CD47-dependent and -independent pro-and anti-inflammatory effects on the IL-1β pathway. Therefore, thrombospondin-1 and its receptor CD47 may be useful targets for limiting the pro-inflammatory effects of lipopolysaccharide and for treating endotoxemia.
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THBS1 is a central mediator of immune modulation and anti-angiogenic signaling in senescent niches.
“THBS1 from senescent fibroblasts was predicted to target macrophages, T/NK cells, and endothelial cells through CD47 and CD36, implicating THBS1 as a central mediator of immune modulation and anti-angiogenic signaling in senescent niches (Figure 6F).64,65,66”
From Cellular senescence in human liver under normal aging and cancer (2026) · cites this paper as [65]
The Discussion (page unavailable) describes TSP1/CD47 signaling as regulating macrophage responses, T-cell activation, and dendritic-cell behavior, supporting the immune-modulation part of the claim. It does not establish THBS1 as a central mediator in senescent niches or address anti-angiogenic signaling there. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTHBS1 from senescent fibroblasts was predicted to target macrophages, T/NK cells, and endothelial cells through CD47 and CD36.
“THBS1 from senescent fibroblasts was predicted to target macrophages, T/NK cells, and endothelial cells through CD47 and CD36, implicating THBS1 as a central mediator of immune modulation and anti-angiogenic signaling in senescent niches (Figure 6F).64,65,66”
From Cellular senescence in human liver under normal aging and cancer (2026) · cites this paper as [65]
The introductory passage labeled Abstract describes TSP1 signaling through CD47 and CD36 in macrophages, supporting the macrophage–receptor part of the claim. The Discussion also distinguishes CD47-mediated effects at physiological TSP1 concentrations from CD36 signaling at higher concentrations. Neither passage reports a prediction involving THBS1 from senescent fibroblasts targeting T/NK or endothelial cells, so the full attributed claim is not supported. (LLM, conf=0.87)
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Self-citationThe circulating immune cell landscape stratifies metastatic burden in breast cancer patientsPreprint
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Chou, T.-Y., Ye, Y.-Z., Lien, C.-J., Wang, J.-C., Yang, C.-H., Chen, Y.-T., Chao, P.-A., & Lin, J.-D. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.07.09.602634
Lin, J.-D., Chou, T.-Y., Ye, Y.-Z., Lin, I.-J., Lien, C.-J., Yang, C.-H., Chen, Y.-T., & Chao, P.-A. (2024) · Research Square · doi:10.21203/rs.3.rs-4707069/v1
- Authors
- Stein, E. V., Miller, T. W., Ivins-O’Keefe, K., Kaur, S., & Roberts, D. D.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Roberts, David D.
- Venue
- Scientific Reports
- Published
- 2016-01-27
- Volume
- 6
- Issue
- 1
- Pages
- 19684-19684
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC4728557
- OpenAlex
- W2259285103
- Cited by
- 115
- References
- 79
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 24 · 2023: 15 · 2022: 9 · 2021: 11 · 2020: 15 · 2019: 2 · 2018: 8 · 2017: 5 · 2016: 2
- FWCI
- 2.95
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- thrombospondin-1, CD47, IL-1β, macrophages, lipopolysaccharide, CD14, NF-κB, AP-1, inflammasome, NLRP3, caspase-1, endotoxemia, inflammation regulation, CD36, integrin-binding domain
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Adenosine Triphosphate, Animals, Cell Line, Humans, Lipopolysaccharides, Macrophage Activation, Macrophages, Models, Biological, Protein Binding, Signal Transduction, Gene Expression, Mice, Knockout, Lipopolysaccharide Receptors, Thrombospondin 1, Caspase 1, Toll-Like Receptor 4, Mice, CD47 Antigen, Interleukin-1beta
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