The DOI matches its Crossref record; 160 of the 166 references it cites were found in a registry or an index.
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]
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“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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Citations
Cites
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BackgroundComplement and microglia mediate early synapse loss in Alzheimer mouse models
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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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