Cited by 237Complement system in diseasesBiomarkers in Disease MechanismsPhagocytosis and Immune Regulation

C1q: A fresh look upon an old molecule

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Thielens, Nicole M., Tedesco, Francesco, Bohlson, Suzanne S., Gaboriaud, Christine, Tenner, Andrea J.·2017·Molecular Immunology

Abstract

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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Crossref · 10.1016/j.molimm.2017.05.025

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  • The existence of redundant mechanisms for clearing apoptotic debris suggests that C1q has an alternative function in maintaining self-tolerance in SLE.

    “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]

    Section 2.4 (page unavailable) describes an immunoregulatory role for C1q beyond debris clearance: it promotes anti-inflammatory responses and limits responses to self-antigens, consistent with maintaining self-tolerance. But the paper does not establish the claimed redundancy of apoptotic-debris clearance mechanisms; it instead describes a predominant role for C1q over C1 activation and C3b deposition in apoptotic-cell clearance and immunosuppression. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • The PIGs module is involved in the activation of the classical complement cascade (GO:0006956), and in effector mechanisms triggered by the complement cascade such as endocytosis (GO:0045807), lysosomal degradation (GO:0005764), antigen processing and presentation (GO:0002474), immune response (GO:0002376), and oxidation-reduction processes (GO:0055114).

    “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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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)
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
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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