The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Complement in disease: a defence system turning offensive
Open accessAbstract
Although the complement system is primarily perceived as a host defence system, a more versatile, yet potentially more harmful side of this innate immune pathway as an inflammatory mediator also exists. The activities that define the ability of the complement system to control microbial threats and eliminate cellular debris — such as sensing molecular danger patterns, generating immediate effectors, and extensively coordinating with other defence pathways — can quickly turn complement from a defence system to an aggressor that drives immune and inflammatory diseases. These host-offensive actions become more pronounced with age and are exacerbated by a variety of genetic factors and autoimmune responses. Complement can also be activated inappropriately, for example in response to biomaterials or transplants. A wealth of research over the past two decades has led to an increasingly finely tuned understanding of complement activation, identified tipping points between physiological and pathological behaviour, and revealed avenues for therapeutic intervention. This Review summarizes our current view of the key activating, regulatory, and effector mechanisms of the complement system, highlighting important crosstalk connections, and, with an emphasis on kidney disease and transplantation, discusses the involvement of complement in clinical conditions and promising therapeutic approaches.
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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
Self-citationControl of adaptive immunity by the innate immune system
Iwasaki, A., & Medzhitov, R. (2015) · Nature Immunology · doi:10.1038/ni.3123 · Cited by 2,160
Hageman, G. S., Anderson, D. H., Johnson, L. V., Hancox, L. S., Taiber, A. J., Hardisty, L. I., Hageman, J. L., Stockman, H. A., Borchardt, J. D., Gehrs, K. M., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0501536102 · Cited by 1,961
Overview of complement activation and regulation
Noris, M., & Remuzzi, G. (2013) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2013.08.001 · Cited by 864
Complement factor H binds malondialdehyde epitopes and protects from oxidative stress
Weismann, D., Hartvigsen, K., Lauer, N., Bennett, K. L., Scholl, H. P. N., Issa, P. C., Cano, M., Brandstätter, H., Tsimikas, S., Skerka, C., et al. (2011) · Nature · doi:10.1038/nature10449 · Cited by 533
Complementing the inflammasome
Triantafilou, M., Hughes, T. R., Morgan, B. P., & Triantafilou, K. (2016) · Immunology · doi:10.1111/imm.12556 · Cited by 76
Complement deficiency promotes cutaneous wound healing in mice
Rafail, S., Kourtzelis, I., Foukas, P. G., Markiewski, M. M., DeAngelis, R. A., Guariento, M., Ricklin, D., Grice, E. A., & Lambris, J. D. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1402354 · Cited by 72
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Cited by
Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases
Lloyd-Price, J., Arze, C., Ananthakrishnan, A. N., Schirmer, M., Avila-Pacheco, J., Poon, T. W., Andrews, E., Ajami, N. J., Bonham, K. S., Brislawn, C. J., et al. (2019) · Nature · doi:10.1038/s41586-019-1237-9 · Cited by 3,143
Ultra-High-Throughput Clinical Proteomics Reveals Classifiers of COVID-19 Infection
Messner, C. B., Demichev, V., Wendisch, D., Michalick, L., White, M., Freiwald, A., Textoris-Taube, K., Vernardis, S. I., Egger, A.-S., Kreidl, M., et al. (2020) · Cell Systems · doi:10.1016/j.cels.2020.05.012 · Cited by 561
Systemic AAV Micro-dystrophin Gene Therapy for Duchenne Muscular Dystrophy
Duan, D. (2018) · Molecular Therapy · doi:10.1016/j.ymthe.2018.07.011 · Cited by 489
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-citationTLR4 Cross-Talk With NLRP3 Inflammasome and Complement Signaling Pathways in Alzheimer's Disease
Yang, J., Wise, L., & Fukuchi, K.-I. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00724 · Cited by 387
Metadata
- Authors
- Ricklin, D., Reis, E. S., & Lambris, J. D.
- Venue
- Nature Reviews Nephrology
- Published
- 2016-05-23
- Volume
- 12
- Issue
- 7
- Pages
- 383-401
- ISSN
- 1745-8323 (ISSN-L)
- 1759-5061
- 1759-507X
- OpenAlex
- W2397512299
- Cited by
- 550
- References
- 7
- FWCI
- 3.90
- 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).
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