The role of multiple toll-like receptor signalling cascades on interactions between biomedical polymers and dendritic cells
Open accessAbstract
Biomaterials are used in several health-related applications ranging from tissue regeneration to antigen-delivery systems. Yet, biomaterials often cause inflammatory reactions suggesting that they profoundly alter the homeostasis of host immune cells such as dendritic cells (DCs). Thus, there is a major need to understand how biomaterials affect the function of these cells. In this study, we have analysed the influence of chemically and physically diverse biomaterials on DCs using several murine knockouts. DCs can sense biomedical polymers through a mechanism, which involves multiple TLR/MyD88-dependent signalling pathways, in particular TLR2, TLR4 and TLR6. TLR-biomaterial interactions induce the expression of activation markers and pro-inflammatory cytokines and are sufficient to confer on DCs the ability to activate antigen-specific T cells. This happens through a direct biomaterial-DC interaction although, for degradable biomaterials, soluble polymer molecules can also alter DC function. Finally, the engagement of TLRs by biomaterials profoundly alters DC adhesive properties. Our findings could be useful for designing structure-function studies aimed at developing more bioinert materials. Moreover, they could also be exploited to generate biomaterials for studying the molecular mechanisms of TLR signalling and DC activation aiming at fine-tuning desired and pre-determined immune responses.
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Being able to control TLR pathways through biomaterials allows control over the behavior of DCs and subsequently the T lymphocyte activation cascade.
“Being able to control TLR pathways through biomaterials also allows control over the behavior of DCs and subsequently the T lymphocyte activation cascade.”
From Unraveling and Harnessing the Immune Response at the Cell–Biomaterial Interface for Tissue Engineering Purposes (2024) · cites this paper as [98]
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- Authors
- Shokouhi, B., Coban, C., Hasirci, V., Aydin, E., Dhanasingh, A., Shi, N., Koyama, S., Akira, S., Zenke, M., & Sechi, A. S.
- Affiliations
- Universitätsklinikum Aachen (DE)
- Immunology Frontier Research Center, The University of Osaka (JP)
- Middle East Technical University (TR)
- RWTH Aachen University (DE)
- Corresponding author
- Sechi, Antonio S.
- ORCID
- Venue
- Biomaterials
- Publisher
- Elsevier BV
- Published
- 2010-08
- Volume
- 31
- Issue
- 22
- Pages
- 5759-5771
- ISSN
- 0142-9612 (ISSN-L)
- OpenAlex
- W2134767971
- Cited by
- 77
- References
- 65
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 1 · 2022: 5 · 2021: 6 · 2020: 10 · 2019: 4 · 2018: 4 · 2017: 9 · 2016: 4 · 2015: 7 · 2014: 1 · 2013: 5 · 2012: 7
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Biomaterials (publishedVersion)
- PubMed (publishedVersion)
- OpenMETU (Middle East Technical University) (submittedVersion, cc-by-nc-nd)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Funders
- RWTH Aachen University
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Keywords
- Toll-like receptors, dendritic cells, biomedical polymers, TLR2, TLR4, TLR6, biomaterial-immune interaction, inflammatory cytokines, T cell activation, dendritic cell adhesion, degradable polymers, bioinert materials
- MeSH terms
- Animals, Biocompatible Materials, Dendritic Cells, Mice, Inbred C57BL, Mice, Knockout, Toll-Like Receptors, Toll-Like Receptor 2, Toll-Like Receptor 4, Toll-Like Receptor 6, Mice, Myeloid Differentiation Factor 88
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