Evidence map›Paper›PMID 25381385›Full record

ArticleJournal of leukocyte biology2015

Complement protein C1q bound to apoptotic cells suppresses human macrophage and dendritic cell-mediated Th17 and Th1 T cell subset proliferation.

Elizabeth V Clarke, Brian M Weist, Craig M Walsh, Andrea J Tenner

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
–field-weighted citation impact
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

62 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Role of Innate Immunity in Cancer.Advances in experimental medicine and biology · 2025
    Review
  7. Complement C1q is a key player in tumor-associated macrophage-mediated CD8International journal of biological sciences · 2024
    Article
  8. Complement C1q essential for aeroallergen sensitization via CSF1RThe Journal of allergy and clinical immunology · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

4 authors.

Elizabeth V ClarkeDepartment of Molecular Biology and Biochemistry, Institute for Immunology, University of California-Irvine, Irvine, California, USA; and.
Brian M WeistDepartment of Molecular & Cell Biology, University of California-Berkeley, Berkeley, California, USA.
Craig M WalshDepartment of Molecular Biology and Biochemistry, Institute for Immunology, University of California-Irvine, Irvine, California, USA; and.
Andrea J TennerDepartment of Molecular Biology and Biochemistry, Institute for Immunology, University of California-Irvine, Irvine, California, USA; and atenner@uci.edu.

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Melanie Funes · 1994 to 2026
$57.9M
Institute for Clinical and Translational ScienceUL1TR000153 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M · 2012 to 2015
$12.1M
INTERACTION OF CLQ ON PHAGOCYTIC CELLSR01AI041090 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI TENNER, ANDREA JOAN · 1996 to 2010
$3.1M
Immunology Research Training ProgramT32AI060573 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI PEARLMAN, ERIC · 2005 to 2020
$1.9M
NCATS NIH HHS UL1 TR000153NCI NIH HHS P30 CA062203NIAID NIH HHS AI-41090NIAID NIH HHS R01 AI041090NIAID NIH HHS T32 AI060573NIAID NIH HHS T32-AI 60573
6 · The paper itself

Abstract

A complete genetic deficiency of the complement protein C1q results in SLE with nearly 100% penetrance in humans, but the molecular mechanisms responsible for this association have not yet been fully determined. C1q opsonizes ACs for enhanced ingestion by phagocytes, such as Mϕ and iDCs, avoiding the extracellular release of inflammatory DAMPs upon loss of the membrane integrity of the dying cell. We previously showed that human monocyte-derived Mϕ and DCs ingesting autologous, C1q-bound LALs (C1q-polarized Mϕ and C1q-polarized DCs), enhance the production of anti-inflammatory cytokines, and reduce proinflammatory cytokines relative to Mϕ or DC ingesting LAL alone. Here, we show that C1q-polarized Mϕ have elevated PD-L1 and PD-L2 and suppressed surface CD40, and C1q-polarized DCs have higher surface PD-L2 and less CD86 relative to Mϕ or DC ingesting LAL alone, respectively. In an MLR, C1q-polarized Mϕ reduced allogeneic and autologous Th17 and Th1 subset proliferation and demonstrated a trend toward increased Treg proliferation relative to Mϕ ingesting LAL alone. Moreover, relative to DC ingesting AC in the absence of C1q, C1q-polarized DCs decreased autologous Th17 and Th1 proliferation. These data demonstrate that a functional consequence of C1q-polarized Mϕ and DC is the regulation of Teff activation, thereby "sculpting" the adaptive immune system to avoid autoimmunity, while clearing dying cells. It is noteworthy that these studies identify novel target pathways for therapeutic intervention in SLE and other autoimmune diseases.

Indexed as

Cell ProliferationApoptosisComplement C1qDendritic CellsFlow CytometryHumansLupus Erythematosus, SystemicLymphocyte ActivationLymphocyte Culture Test, MixedMacrophagesPhagocytosisTh17 CellsTh1 CellsComplement C1qautoimmunityinflammationphagocytosis

Identifiers

PMID25381385
PMCPMC4377823

What OpenQuestion holds

Textmetadata
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.