Evidence map›Paper›PMID 18820683›Full record

ArticleNature immunology2008

Modulation of the antitumor immune response by complement.

Maciej M Markiewski, Robert A DeAngelis, Fabian Benencia, Salome K Ricklin-Lichtsteiner, Anna Koutoulaki, Craig Gerard, George Coukos, John D Lambris

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 430 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
430citing papers in PubMed, 1 pooled it
10.9field-weighted citation impact, top 1% 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

430 citing papers in PubMed, 1 synthesis or guideline pooled it, 761 citations in OpenAlex.

  1. Immune cells mediate the causal pathway linking circulating complements to cancer: A Mendelian randomization study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Pooled it
  2. Trial
  3. Article
  4. Towards liquid biopsy-based analysis of antitumour immunity.Nature reviews. Clinical oncology · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Bioorthogonal tuning of nanosurface opsonisationChemical communications (Cambridge, England) · 2026
    Article
  11. Article
  12. Liposomes in tumor treatment: a double-edged sword.Science China. Life sciences · 2026
    Review
  13. Article
  14. Review
  15. Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Maciej M MarkiewskiDepartment of Pathology and Laboratory Medicine, Medical School of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Robert A DeAngelis
Fabian Benencia
Salome K Ricklin-Lichtsteiner
Anna Koutoulaki
Craig Gerard
George Coukos
John D Lambris
University of Pennsylvania · USBoston Children's Hospital · USWestern University of Health Sciences · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
STRUCTURAL-FUNCTIONAL ANALYSIS OF COMPSTATINR01GM062134 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2001 to 2010
$2.5M
The role of complement in ovarian cancerR01CA112162 · NCI · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2005 to 2009
$1.5M
NCI NIH HHS R01 CA112162NIAID NIH HHS P01 AI068730NIGMS NIH HHS GM62134NIGMS NIH HHS R01 GM062134PHS HHS A1068730
6 · The paper itself

Abstract

The involvement of complement-activation products in promoting tumor growth has not yet been recognized. Here we show that the generation of complement C5a in a tumor microenvironment enhanced tumor growth by suppressing the antitumor CD8(+) T cell-mediated response. This suppression was associated with the recruitment of myeloid-derived suppressor cells into tumors and augmentation of their T cell-directed suppressive abilities. Amplification of the suppressive capacity of myeloid-derived suppressor cells by C5a occurred through regulation of the production of reactive oxygen and nitrogen species. Pharmacological blockade of the C5a receptor considerably impaired tumor growth to a degree similar to the effect produced by the anticancer drug paclitaxel. Thus, our study demonstrates a therapeutic function for complement inhibition in the treatment of cancer.

Indexed as

Immunosuppression TherapyAnimalsComplement ActivationComplement C3-C5 ConvertasesComplement C5aDown-RegulationFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMyeloid CellsNeoplasmsReactive Nitrogen SpeciesReactive Oxygen SpeciesComplement C3-C5 ConvertasesComplement C5aReactive Nitrogen SpeciesReactive Oxygen SpeciesReceptor, Anaphylatoxin C5a

Identifiers

PMID18820683
PMCPMC2678913
OpenAlexW2076936113

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.