The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
The Where, When, How, and Why of Hyaluronan Binding by Immune Cells
Open accessAbstract
Hyaluronan is made and extruded from cells to form a pericellular or extracellular matrix (ECM) and is present in virtually all tissues in the body. The size and form of hyaluronan present in tissues are indicative of a healthy or inflamed tissue, and the interactions of hyaluronan with immune cells can influence their response. Thus, in order to understand how inflammation is regulated, it is necessary to understand these interactions and their consequences. Although there is a large turnover of hyaluronan in our bodies, the large molecular mass form of hyaluronan predominates in healthy tissues. Upon tissue damage and/or infection, the ECM and hyaluronan are broken down and an inflammatory response ensues. As inflammation is resolved, the ECM is restored, and high molecular mass hyaluronan predominates again. Immune cells encounter hyaluronan in the tissues and lymphoid organs and respond differently to high and low molecular mass forms. Immune cells differ in their ability to bind hyaluronan and this can vary with the cell type and their activation state. For example, peritoneal macrophages do not bind soluble hyaluronan but can be induced to bind after exposure to inflammatory stimuli. Likewise, naïve T cells, which typically express low levels of the hyaluronan receptor, CD44, do not bind hyaluronan until they undergo antigen-stimulated T cell proliferation and upregulate CD44. Despite substantial knowledge of where and when immune cells bind hyaluronan, why immune cells bind hyaluronan remains a major outstanding question. Here, we review what is currently known about the interactions of hyaluronan with immune cells in both healthy and inflamed tissues and discuss how hyaluronan binding by immune cells influences the inflammatory response.
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Cites
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Oligosaccharides of Hyaluronan Activate Dendritic Cells via Toll-like Receptor 4
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Hyaluronan as an Immune Regulator in Human Diseases
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Hyaluronan Fragments Act as an Endogenous Danger Signal by Engaging TLR2
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Hyaluronan Fragments Stimulate Endothelial Recognition of Injury through TLR4
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Hyaluronan, a Crucial Regulator of Inflammation
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Fibroblast migration is mediated by CD44-dependent TGFβ activation
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Enhanced deposition of low-molecular-weight hyaluronan in lungs of cigarette smoke-exposed mice
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Staphylococcus aureus Secreted Toxins and Extracellular Enzymes
Tam, K., & Torres, V. J. (2019) · Microbiology Spectrum · doi:10.1128/microbiolspec.gpp3-0039-2018 · Cited by 452
Bhattacharjee, S., Hamberger, F., Ravichandra, A., Miller, M., Nair, A., Affo, S., Filliol, A., Chin, L., Savage, T. M., Yin, D., et al. (2021) · Journal of Clinical Investigation · doi:10.1172/jci146987 · Cited by 367
Biglycan, a novel trigger of Th1 and Th17 cell recruitment into the kidney
Nastase, M. V., Zeng-Brouwers, J., Beckmann, J., Tredup, C., Christen, U., Radeke, H. H., Wygrecka, M., & Schaefer, L. (2018) · Matrix Biology · doi:10.1016/j.matbio.2017.12.002 · Cited by 60
The role of hyaluronan in renal cell carcinoma
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Metadata
- Authors
- Lee-Sayer, S. S. M., Dong, Y., Arif, A. A., Olsson, M., Brown, K. L., & Johnson, P.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2015-04-14
- Volume
- 6
- Pages
- 150-150
- ISSN
- 1664-3224 (ISSN-L)
- OpenAlex
- W2151898179
- Cited by
- 184
- References
- 10
- FWCI
- 6.32
- Type
- journal article
- Language
- en
- Open access
- gold
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- Lee-Sayer, S. S. M., Dong, Y., Arif, A. A., Olsson, M., Brown, K. L., & Johnson, P. (2015). The Where, When, How, and Why of Hyaluronan Binding by Immune Cells. Frontiers in Immunology. https://doi.org/10.3389/fimmu.2015.00150
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