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Complement and its role in innate and adaptive immune responses
Abstract
The complement system plays a crucial role in the innate defense against common pathogens. Activation of complement leads to robust and efficient proteolytic cascades, which terminate in opsonization and lysis of the pathogen as well as in the generation of the classical inflammatory response through the production of potent proinflammatory molecules. More recently, however, the role of complement in the immune response has been expanded due to observations that link complement activation to adaptive immune responses. It is now appreciated that complement is a functional bridge between innate and adaptive immune responses that allows an integrated host defense to pathogenic challenges. As such, a study of its functions allows insight into the molecular underpinnings of host-pathogen interactions as well as the organization and orchestration of the host immune response. This review attempts to summarize the roles that complement plays in both innate and adaptive immune responses and the consequences of these interactions on host defense.
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“We identified and annotated 61 genes in the muskox MHC Class III region, including members of the TNF family123,124, the Lymphocyte Antigen-6 family members125, and the members of the complement cascade.126”
From Chromosomal-level reference genome assembly of muskox (Ovibos moschatus) from Banks Island in the Canadian Arctic, a resource for conservation genomics (2024) · cites this paper as [126]
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“MASP1, activated by the lectin complement pathway which is initiated by the binding of mannose-binding lectin to bacterial surfaces with mannose-containing polysaccharides [51]”
In the citing paper
“an overactive complement system, a vital element of the immune system that enhances the opsonization of pathogens and initiates a series of inflammatory responses to help fight infection [51].”
In the citing paper
“This overreaction of the innate immune system against viral infection induces the so-called “cytokine storm””
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [40]
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Metadata
- Authors
- Dunkelberger, J. R., & Song, W.-C.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- Song, Wen-Chao
- ORCID
- Song, Wen-Chao
- Venue
- Cell Research
- Published
- 2009-12-15
- Volume
- 20
- Issue
- 1
- Pages
- 34-50
- ISSN
- 1001-0602 (ISSN-L)
- 1748-7838
- OpenAlex
- W2005044790
- Cited by
- 1,932
- References
- 170
- Citations by year
- 2026: 163 · 2025: 207 · 2024: 239 · 2023: 192 · 2022: 149 · 2021: 186 · 2020: 103 · 2019: 85 · 2018: 103 · 2017: 98 · 2016: 95 · 2015: 67 · 2014: 65 · 2013: 49 · 2012: 68
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- complement system, innate immunity, adaptive immunity, complement activation, opsonization, proinflammatory molecules, host-pathogen interaction
- MeSH terms
- Animals, B-Lymphocytes, Complement System Proteins, Humans, Immunity, Innate, Inflammation, T-Lymphocytes, Inflammation Mediators, Host-Pathogen Interactions, Adaptive Immunity, Immunity, Humoral
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