The DOI matches its Crossref record; 87 of the 87 references it cites were found in a registry or an index.
Complement in Immune and Inflammatory Disorders: Pathophysiological Mechanisms
Open accessAbstract
Although acute or chronic inflammation is a common component of many clinical disorders, the underlying processes can be highly distinct. In recent years, the complement system has been associated with a growing number of immunological and inflammatory conditions that include degenerative diseases, cancer, and transplant rejection. It becomes evident that excessive activation or insufficient control of complement activation on host cells can cause an immune imbalance that may fuel a vicious cycle between complement, inflammatory cells, and tissue damage that exacerbates clinical complications. Although the exact involvement of complement needs to be carefully investigated for each disease, therapeutic modulation of complement activity emerges as an attractive target for upstream inhibition of inflammatory processes. This review provides an update about the functional and collaborative capabilities of complement, highlights major disease areas with known complement contribution, and indicates the potential for complement as a focal point in immunomodulatory strategies for treating inflammatory diseases.
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Citations
Cites
Complement: a key system for immune surveillance and homeostasis
Ricklin, D., Hajishengallis, G., Yang, K., & Lambris, J. D. (2010) · Nature Immunology · doi:10.1038/ni.1923 · Cited by 3,654 · cited 9×
“The cross-talk between TLR, CD14, and MyD88 on the Toll side and complement components including C5aR, CR3, CD46, CD55, and gC1qR is important for antimicrobial defense but also contributes to inflammatory disorders (24).”
BackgroundInfluentialSelf-citationHematological Problems in Pediatric Intensive Care
Revel-Vilk, S., Cox, P., Robitaille, N., & Blanchette, V. (2014) · Pediatric and Adolescent Medicine · doi:10.1159/000350346 · Cited by 3,508
Non-Transgenic Mouse Models of Kidney Disease
Rabe, M., & Schaefer, F. (2016) · Nephron · doi:10.1159/000445171 · Cited by 1,922
Modulation of the antitumor immune response by complement
Markiewski, M. M., DeAngelis, R. A., Benencia, F., Ricklin-Lichtsteiner, S. K., Koutoulaki, A., Gerard, C., Coukos, G., & Lambris, J. D. (2008) · Nature Immunology · doi:10.1038/ni.1655 · Cited by 778
Self-citationThe role of the anaphylatoxins in health and disease
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Anderson, D. H., Radeke, M. J., Gallo, N. B., Chapin, E. A., Johnson, P. T., Curletti, C. R., Hancox, L. S., Hu, J., Ebright, J. N., Malek, G., et al. (2010) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2009.11.003 · Cited by 727
The Role of Complement in Inflammatory Diseases From Behind the Scenes into the Spotlight
Markiewski, M. M., & Lambris, J. D. (2007) · The American Journal of Pathology · doi:10.2353/ajpath.2007.070166 · Cited by 722
Self-citationMolecular Intercommunication between the Complement and Coagulation Systems
Amara, U., Flierl, M. A., Rittirsch, D., Klos, A., Chen, H., Acker, B., Brückner, U. B., Nilsson, B., Gebhard, F., Lambris, J. D., et al. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0903678 · Cited by 720
Self-citationAtypical hemolytic uremic syndrome
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Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome
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Self-citation
Cited by
Lian, H., Yang, L., Cole, A., Sun, L., Chiang, A. C.-A., Fowler, S. W., Shim, D. J., Rodriguez-Rivera, J., Taglialatela, G., Jankowsky, J. L., et al. (2015) · Neuron · doi:10.1016/j.neuron.2014.11.018 · Cited by 697
Complement component C3 – The “Swiss Army Knife” of innate immunity and host defense
Ricklin, D., Reis, E. S., Mastellos, D. C., Gros, P., & Lambris, J. D. (2016) · Immunological Reviews · doi:10.1111/imr.12500 · Cited by 484
Self-citationCell-specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain
Fonseca, M. I., Chu, S.-H., Hernandez, M. X., Fang, M. J., Modarresi, L., Selvan, P., MacGregor, G. R., & Tenner, A. J. (2017) · Journal of Neuroinflammation · doi:10.1186/s12974-017-0814-9 · Cited by 337
ApoE attenuates unresolvable inflammation by complex formation with activated C1q
Yin, C., Ackermann, S., Ma, Z., Mohanta, S. K., Zhang, C., Li, Y., Nietzsche, S., Westermann, M., Peng, L., Hu, D., et al. (2019) · Nature Medicine · doi:10.1038/s41591-018-0336-8 · Cited by 305
Veneman, W. J., Spaink, H. P., Brun, N. R., Bosker, T., & Vijver, M. G. (2017) · Aquatic Toxicology · doi:10.1016/j.aquatox.2017.06.014 · Cited by 204
Metadata
- Authors
- Ricklin, D., & Lambris, J. D.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-04
- Volume
- 190
- Issue
- 8
- Pages
- 3831-3838
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2156022583
- Cited by
- 478
- References
- 87
- FWCI
- 22.50
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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