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C1q: A fresh look upon an old molecule
Open accessAbstract
Originally discovered as part of C1, the initiation component of the classical complement pathway, it is now appreciated that C1q regulates a variety of cellular processes independent of complement activation. C1q is a complex glycoprotein assembled from 18 polypeptide chains, with a C-terminal globular head region that mediates recognition of diverse molecular structures, and an N-terminal collagen-like tail that mediates immune effector mechanisms. C1q mediates a variety of immunoregulatory functions considered important in the prevention of autoimmunity such as the enhancement of phagocytosis, regulation of cytokine production by antigen presenting cells, and subsequent alteration in T-lymphocyte maturation. Furthermore, recent advances indicate additional roles for C1q in diverse physiologic and pathologic processes including pregnancy, tissue repair, and cancer. Finally, C1q is emerging as a critical component of neuronal network refinement and homeostatic regulation within the central nervous system. This review summarizes the classical functions of C1q and reviews novel discoveries within the field.
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“the existence of redundant mechanisms in clearing apoptotic debris, including those mediated by C3 and complement activation independent of C1q79,80, suggest that C1q has an alternative function in maintaining self-tolerance in SLE”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [80]
Experimental — accuracy not yet measuredIn the citing paper
“Based on the ontology analysis (Table S4), we conclude that the module is involved in the activation of the classical complement cascade (GO:0006956, i.e. C1qa, C1qb, C1qc, C4a, C4b ), but also in effector mechanisms triggered by the complement cascade (Schmidt and Gessner, 2005; Thielens et al. , 2017) such as endocytosis (GO:0045807, i.e. Fcer1g, Fcgr3, B2m, Cd63, Cyba, Apoe,”
From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as Thielens et al., 2017
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“As described above, C1q has long been recognized as initiator of the classical pathway of complement (C) activation and its tissue deposition when co-localized with C4 and C3 was usually regarded as an indication of local C activation (Ricklin et al., 2010; Merle et al., 2015).”
BackgroundComplement and microglia mediate early synapse loss in Alzheimer mouse models
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BackgroundThe Classical Complement Cascade Mediates CNS Synapse Elimination
Stevens, B., Allen, N. J., Vazquez, L. E., Howell, G. R., Christopherson, K. S., Nouri, N., Micheva, K. D., Mehalow, A. K., Huberman, A. D., Stafford, B., et al. (2007) · Cell · doi:10.1016/j.cell.2007.10.036 · Cited by 3,313
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Self-citation
Metadata
- Authors
- Thielens, N. M., Tedesco, F., Bohlson, S. S., Gaboriaud, C., & Tenner, A. J.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- IRCCS Istituto Auxologico Italiano (IT)
- Des Moines University (US)
- University of California, Irvine (US)
- Corresponding author
- Thielens, Nicole M.
- Tenner, Andrea J.
- Venue
- Molecular Immunology
- Publisher
- Elsevier BV
- Published
- 2017-09
- Volume
- 89
- Pages
- 73-83
- ISSN
- 0161-5890 (ISSN-L)
- PMC
- PMC5582005
- OpenAlex
- W2622909676
- Cited by
- 237
- References
- 166
- Citations by year
- 2026: 15 · 2025: 21 · 2024: 25 · 2023: 16 · 2022: 33 · 2021: 34 · 2020: 32 · 2019: 32 · 2018: 25 · 2017: 3
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Molecular Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- French National Research Agency (ANR-09-PIRI-0021)
- CG,NMT (ANR-16-CE11-0019-01)
- AJT (NIH AG00536)
- SSB (NIH NIAID 1R15AI117474)
- 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 › Phagocytosis and Immune Regulation
- Keywords
- C1q, classical complement pathway, complement regulation, immune regulation, autoimmunity, phagocytosis, antigen-presenting cells, cytokine production, T cell development, pregnancy, tissue repair, cancer, CNS homeostasis
- MeSH terms
- Cell Physiological Phenomena, Central Nervous System, Homeostasis, Humans, Immunity, Innate, Models, Molecular, Nerve Net, Complement C1q, Protein Structure, Quaternary, Adaptive Immunity
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