Evidence map›Paper›PMID 17607007›Full record

ReviewProceedings of the American Thoracic Society2007

Complement activation pathways: a bridge between innate and adaptive immune responses in asthma.

Marsha Wills-Karp

Open access · greenAbstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Effective delivery of miR-511-3p with mannose-decorated exosomes with RNA nanoparticles confers protection against asthma.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Article
  5. Article
  6. Article
  7. Overexpression of Decay Accelerating Factor Mitigates Fibrotic Responses to Lung Injury.American journal of respiratory cell and molecular biology · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Osteoarthritis and the Complement Cascade.Clinical medicine insights. Arthritis and musculoskeletal disorders · 2018
    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

1 author at 1 institution in 1 country.

Marsha Wills-KarpDivision of Immunobiology,Center for Immunological Research, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio 45229, USA. wildc7@cchmc.org
Cincinnati Children's Hospital Medical Center · US

Funding

Unique Effects of IL-13 in Asthma: Mechanistic AnalysisP01HL076383 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI FINKELMAN, FRED DOUGLASS · 2004 to 2008
$10.1M
Asthma Positional Candidate Genes in Mice and HumansR01HL067736 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLS-KARP, MARSHA · 2000 to 2010
$4.1M
NHLBI NIH HHS HL076383NHLBI NIH HHS HL67736
6 · The paper itself

Abstract

Although it is widely accepted that allergic asthma is driven by T helper type 2 (Th2)-polarized immune responses to innocuous environmental allergens, the mechanisms driving these aberrant immune responses remain elusive. Recent recognition of the importance of innate immune pathways in regulating adaptive immune responses have fueled investigation into the role of innate immune pathways in the pathogenesis of asthma. The phylogenetically ancient innate immune system, the complement system, is no exception. The emerging paradigm is that C3a production at the airway surface serves as a common pathway for the induction of Th2-mediated inflammatory responses to a variety of environmental triggers of asthma (i.e., allergens, pollutants, viral infections, cigarette smoke). In contrast, C5a plays a dual immunoregulatory role by protecting against the initial development of a Th2-polarized adaptive immune response via its ability to induce tolerogenic dendritic cell subsets. On the other hand, C5a drives type 2-mediated inflammatory responses once inflammation ensues. Thus, alterations in the balance of generation of the various components of the complement pathway either due to environmental exposure changes or genetic alterations in genes of the complement cascade may underlie the recent rise in asthma prevalence in westernized countries.

Indexed as

Immunity, InnateAnimalsAsthmaComplement ActivationDendritic CellsHumansTh2 CellsToll-Like ReceptorsToll-Like Receptors

Identifiers

PMID17607007
PMCPMC2647626
OpenAlexW1971986054

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.