The extracellular matrix protein mindin is a pattern-recognition molecule for microbial pathogens
Abstract
Microbial pathogens use a variety of their surface molecules to bind to host extracellular matrix (ECM) components to establish an effective infection. However, ECM components can also serve as an integral part of the innate immunity. Mice lacking expression of mindin (spondin 2), a highly conserved ECM protein, have an impaired ability to clear bacterial infection, and mindin-deficient macrophages show defective responses to a broad spectrum of microbial stimuli. Moreover, mindin binds directly to bacteria and their components and functions as an opsonin for macrophage phagocytosis of bacteria. Thus, mindin is essential in the initiation of the innate immune response and represents a unique pattern-recognition molecule in the ECM for microbial pathogens.
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Other inflammation-related genes dysregulated in hEDS/HSD include SPON2 up-regulated and PRLR decreased.
“Other inflammation-related genes dysregulated in hEDS/HSD include SPON2, up-regulated in patients’ cells, which encodes an ECM protein with multifunctional properties in the innate immune system and inflammatory cell recruitment [152,153,154], and PRLR, showing a decreased expression in hEDS/HSD cells, which encode the prolactin receptor implicated in inflammatory responses and immune cells”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [152]
SPON2 encodes an ECM protein with multifunctional properties in the innate immune system and inflammatory cell recruitment.
“Other inflammation-related genes dysregulated in hEDS/HSD include SPON2, up-regulated in patients’ cells, which encodes an ECM protein with multifunctional properties in the innate immune system and inflammatory cell recruitment [152,153,154], and PRLR, showing a decreased expression in hEDS/HSD cells, which encode the prolactin receptor implicated in inflammatory responses and immune cells”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [152]
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- Authors
- He, Y.-W., Li, H., Zhang, J., Hsu, C.-L., Lin, E., Zhang, N., Guo, J., Forbush, K. A., & Bevan, M. J.
- Affiliations
- Duke University (US)
- Duke Medical Center (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- He, You-Wen
- Bevan, Michael J
- Venue
- Nature Immunology
- Published
- 2003-12-14
- Volume
- 5
- Issue
- 1
- Pages
- 88-97
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2072110323
- Cited by
- 171
- References
- 52
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 2 · 2023: 5 · 2022: 9 · 2021: 10 · 2020: 15 · 2019: 7 · 2018: 7 · 2017: 8 · 2016: 5 · 2015: 8 · 2014: 3 · 2013: 4 · 2012: 9
- FWCI
- 2.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01 AI54685)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Keywords
- mindin, extracellular matrix, pattern recognition receptors, innate immunity, macrophage phagocytosis, opsonization, bacterial infection, host-pathogen interaction, macrophages
- MeSH terms
- Amino Acid Sequence, Animals, Extracellular Matrix, Female, Gram-Negative Bacteria, Gram-Positive Bacteria, Humans, Lipopolysaccharides, Male, Mice, Inbred C57BL, Molecular Sequence Data, Teichoic Acids, Cytokines, Extracellular Matrix Proteins, Gram-Negative Bacterial Infections, Gram-Positive Bacterial Infections, Macrophages, Peritoneal, Mice, Knockout, Mice
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