Evidence map›Paper›PMID 31739194›Full record

ArticleMolecular immunology2020

Recombinant C1q variants modulate macrophage responses but do not activate the classical complement pathway.

Victoria Espericueta, Ayla O Manughian-Peter, Isabelle Bally, Nicole M Thielens, Deborah A Fraser

Open access · greenAbstract read
In one paragraph

Article in Molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Journal of inflammation research · 2026
    Article
  2. Article
  3. Article
  4. Novel FABP4Cell death & disease · 2024
    Article
  5. Article
  6. Article
  7. The role of secreted proteins in efferocytosis.Frontiers in cell and developmental biology · 2023
    Review
  8. Article
  9. Article
  10. C1q as a potential tolerogenic therapeutic in transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021
    Article
  11. Article
  12. Article
  13. SLE: Novel Postulates for Therapeutic Options.Frontiers in immunology · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Victoria EspericuetaDepartment of Biological Sciences, California State University Long Beach, CA, USA.
Ayla O Manughian-PeterDepartment of Biological Sciences, California State University Long Beach, CA, USA.
Isabelle BallyUniv. Grenoble Alpes, CEA, CNRS, IBS, F-38000, Grenoble, France.
Nicole M ThielensUniv. Grenoble Alpes, CEA, CNRS, IBS, F-38000, Grenoble, France.
Deborah A FraserDepartment of Biological Sciences, California State University Long Beach, CA, USA. Electronic address: Deborah.fraser@csulb.edu.
University of California, Los Angeles · USCalifornia State University, Long Beach · USCEA Grenoble · FRInstitut de Biologie Structurale · FR

Funding

CSULB Building Biomedical Research Program: Overall ComponentUL1GM118979 · NIGMS · CALIFORNIA STATE UNIVERSITY LONG BEACH · PI CHUN, CHI-AH, DILLON, JESSE · 2015 to 2023
$20.7M
CSULB Building Biomedical Research Program: Student Training CoreTL4GM118980 · NIGMS · CALIFORNIA STATE UNIVERSITY LONG BEACH · PI CHUN, CHI-AH, DILLON, JESSE · 2015 to 2023
$12.3M
CSULB Building Biomedical Research Program: Research Enrichment CoreRL5GM118978 · NIGMS · CALIFORNIA STATE UNIVERSITY LONG BEACH · PI CHUN, CHI-AH, DILLON, JESSE · 2015 to 2023
$7.3M
Complement Protein C1q in AtherosclerosisSC3GM111146 · NIGMS · CALIFORNIA STATE UNIVERSITY LONG BEACH · PI FRASER, DEBORAH ANN · 2014 to 2022
$878k
NIGMS NIH HHS RL5 GM118978NIGMS NIH HHS SC3 GM111146NIGMS NIH HHS TL4 GM118980NIGMS NIH HHS UL1 GM118979
6 · The paper itself

Abstract

Complement protein C1q plays a dual role in a number of inflammatory diseases such as atherosclerosis. While in later stages classical complement pathway activation by C1q exacerbates disease progression, C1q also plays a beneficial role in early disease. Independent of its role in complement activation, we and others have identified a number of potentially beneficial interactions of C1q with phagocytes in vitro, including triggering phagocytosis of cellular and molecular debris and polarizing macrophages toward an anti-inflammatory phenotype. These interactions may also be important in preventing autoimmunity. Here, we characterize variants of recombinant human C1q (rC1q) which no longer initiate complement activation, through mutation of the C1r

Indexed as

Complement C1qComplement Pathway, ClassicalHumansMacrophagesPhagocytosisRecombinant ProteinsComplement C1qRecombinant ProteinsC1qComplementInflammationMacrophagePhagocytosis

Identifiers

PMID31739194
PMCPMC6931381
OpenAlexW2983411840

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.