The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Toll‐like receptors, endogenous ligands, and systemic autoimmune disease
Abstract
Summary: The critical role of Toll‐like receptors (TLRs) as mediators of pathogen recognition by the innate immune system is now firmly established. Such recognition results in the initiation of an inflammatory immune response and subsequent instruction of the adaptive immune system, both of which are designed to rid the host of the invading pathogen. More controversial is the potential role of TLRs in the recognition of endogenous ligands and what effect this might have on the consequent development of autoimmune or other chronic sterile inflammatory disorders. An increasing number of studies implicate TLRs as being involved in the immune response to self‐molecules that have in some way been altered from their native state or accumulate in non‐physiologic sites or amounts, although questions have been raised about possible contaminants in certain of these studies. In this review, we discuss the evidence for endogenous ligand–TLR interactions with particular emphasis on mammalian chromatin, systemic lupus erythematosus, and atherosclerosis. Overall, the data support the general concept of a role for TLRs in the recognition of endogenous ligands. However, the precise details of the interactions and the extent to which they may contribute to the pathogenesis of human disease remain to be clarified.
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Citations
Cites
Inflammation in atherosclerosis
Libby, P. (2002) · Nature · doi:10.1038/nature01323 · Cited by 8,315
A Toll-like receptor recognizes bacterial DNA
Hemmi, H., Takeuchi, O., Kawai, T., Kaisho, T., Sato, S., Sanjo, H., Matsumoto, M., Hoshino, K., Wagner, H., Takeda, K., et al. (2000) · Nature · doi:10.1038/35047123 · Cited by 6,491 · cited 3×
“Furthermore, TLR9 had been reported to recognize bacterial DNA as well as oligodeoxynucleotides (ODN) containing the CpG motifs responsible for the activating capacity of bacterial DNA (CpG s-ODN) (53, 54).”
BackgroundResultTakeda, K., Kaisho, T., & Akira, S. (2003) · Annual Review of Immunology · doi:10.1146/annurev.immunol.21.120601.141126 · Cited by 6,143
Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3
Alexopoulou, L., Holt, A. C., Medzhitov, R., & Flavell, R. A. (2001) · Nature · doi:10.1038/35099560 · Cited by 6,129
Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA
Diebold, S. S., Kaisho, T., Hemmi, H., Akira, S., & Reis e Sousa, C. (2004) · Science · doi:10.1126/science.1093616 · Cited by 3,444
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
mRNA is an endogenous ligand for toll-like receptor 3
Karikó, K., Ni, H., Capodici, J., Lamphier, M., & Weissman, D. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m310175200 · Cited by 1,062
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Autoimmune Disease and Impaired Uptake of Apoptotic Cells in MFG-E8-Deficient Mice
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Björkbacka, H., Kunjathoor, V. V., Moore, K. J., Koehn, S., Ordija, C. M., Lee, M. A., Means, T., Halmen, K., Luster, A. D., Golenbock, D. T., et al. (2004) · Nature Medicine · doi:10.1038/nm1008 · Cited by 634
Cited by
Recognition of microorganisms and activation of the immune response
Medzhitov, R. (2007) · Nature · doi:10.1038/nature06246 · Cited by 2,862
Toll-like receptors in systemic autoimmune disease
Marshak-Rothstein, A. (2006) · Nature Reviews Immunology · doi:10.1038/nri1957 · Cited by 1,116
Self-citationPathogen recognition by innate immunity and its signaling
AKIRA, S. (2009) · Proceedings of the Japan Academy, Series B · doi:10.2183/pjab.85.143 · Cited by 240
Lartigue, A., Courville, P., Auquit, I., François, A., Arnoult, C., Tron, F., Gilbert, D., & Musette, P. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.2.1349 · Cited by 165
Wilson, N. S., Young, L. J., Kupresanin, F., Naik, S. H., Vremec, D., Heath, W. R., Akira, S., Shortman, K., Boyle, J., Maraskovsky, E., et al. (2008) · Immunology & Cell Biology · doi:10.1038/sj.icb.7100125 · Cited by 102
Metadata
- Authors
- Rifkin, I. R., Leadbetter, E. A., Busconi, L., Viglianti, G., & Marshak‐Rothstein, A.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2005-03-16
- Volume
- 204
- Issue
- 1
- Pages
- 27-42
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2081866939
- Cited by
- 389
- References
- 12
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- closed
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- Rifkin, I. R., Leadbetter, E. A., Busconi, L., Viglianti, G., & Marshak‐Rothstein, A. (2005). Toll‐like receptors, endogenous ligands, and systemic autoimmune disease. Immunological Reviews. https://doi.org/10.1111/j.0105-2896.2005.00239.x
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