The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
The role of Toll-like receptors in rheumatoid arthritis
Open accessAbstract
AbtractAn increasing body of data supports the role of the innate immune system in the pathogenesis of rheumatoid arthritis (RA). Toll-like receptors (TLRs) are expressed by cells within the RA joint and various endogenous TLR ligands are present within the inflamed joints of patients with RA. Further, various animal models suggest that TLR signaling is important in the pathogenesis of disease. Overall, the data suggest that activation by endogenous TLR ligands may contribute to the persistent expression of proinflammatory cytokines by macrophages and the joint damage to cartilage and bone that occurs in RA. The data support a potential role for suppression of TLR signaling as a novel therapeutic approach in patients with RA.
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Cites
Oligosaccharides of Hyaluronan Activate Dendritic Cells via Toll-like Receptor 4
Termeer, C., Benedix, F., Sleeman, J., Fieber, C., Voith, U., Ahrens, T., Miyake, K., Freudenberg, M., Galanos, C., & Simon, J. C. (2002) · The Journal of Experimental Medicine · doi:10.1084/jem.20001858 · Cited by 1,378
Therapeutic targeting of innate immunity with Toll-like receptor agonists and antagonists
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Schaefer, L., Babelova, A., Kiss, E., Hausser, H.-J., Baliova, M., Krzyzankova, M., Marsche, G., Young, M. F., Mihalik, D., Götte, M., et al. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23755 · Cited by 850
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“These pathways include the induction of A20 that suppresses NF-κB activation [34], ATF3 that attenuates activation by NF-κB and C/EBPδ [35], and induction of the microRNA miR- 9, which is induced by TLR2 and TLR7/8 agonists and provides feedback suppression of NF-κB activation [ 36 ].”
BackgroundAbdollahi-Roodsaz, S., Joosten, L. A. B., Koenders, M. I., Devesa, I., Roelofs, M. F., Radstake, T. R. D. J., Heuvelmans-Jacobs, M., Akira, S., Nicklin, M. J. H., Ribeiro-Dias, F., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci32639 · Cited by 527
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Cutting Edge: TLR2 Is a Functional Receptor for Acute-Phase Serum Amyloid A
Cheng, N., He, R., Tian, J., Ye, P. P., & Ye, R. D. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.181.1.22 · Cited by 284
Cited by
Aliyu, M., Zohora, F. T., Anka, A. U., Ali, K., Maleknia, S., Saffarioun, M., & Azizi, G. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.109130 · Cited by 401
Matmati, M., Jacques, P., Maelfait, J., Verheugen, E., Kool, M., Sze, M., Geboes, L., Louagie, E., Guire, C. M., Vereecke, L., et al. (2011) · Nature Genetics · doi:10.1038/ng.874 · Cited by 290
Bhattaram, P., & Chandrasekharan, U. (2017) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2016.05.009 · Cited by 136
Al-Riyami, L., Pineda, M. A., Rzepecka, J., Huggan, J. K., Khalaf, A. I., Suckling, C. J., Scott, F. J., Rodgers, D. T., Harnett, M. M., & Harnett, W. (2013) · Journal of Medicinal Chemistry · doi:10.1021/jm401251p · Cited by 94
Kim, N., Choi, S., Han, E., Hong, B., Choi, S. Y., Kwon, H. M., Hwang, S., Cho, C., & Kim, W. (2014) · European Journal of Immunology · doi:10.1002/eji.201343669 · Cited by 48
Metadata
- Authors
- Huang, Q.-Q., & Pope, R. M.
- Venue
- Current Rheumatology Reports
- Published
- 2009-10
- Volume
- 11
- Issue
- 5
- Pages
- 357-364
- ISSN
- 1523-3774 (ISSN-L)
- 1534-6307
- OpenAlex
- W1967601848
- Cited by
- 246
- References
- 7
- FWCI
- 7.61
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
