Evidence map›Paper›PMID 16091207›Full record

ReviewCurrent allergy and asthma reports2005

New insights into the role of the complement pathway in allergy and asthma.

Marsha Wills-Karp, Joerg Koehl

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current allergy and asthma reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. A complex role for complement in allergic asthma.Expert review of clinical immunology · 2010
    Review
  10. Review
  11. Article
  12. Article
  13. Complement 5a receptor inhibition improves renal allograft survival.Journal of the American Society of Nephrology : JASN · 2008
    Article
  14. Identification of a transcriptional fingerprint of estrogen exposure in rainbow trout liver.Toxicological sciences : an official journal of the Society of Toxicology · 2008
    Article
  15. Article
  16. 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

2 authors at 2 institutions in 1 country.

Marsha Wills-KarpDivision of Immunobiology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA. wildc7@chmcc.org
Joerg Koehl
Boston Children's Hospital · USCincinnati Children's Hospital Medical Center · US

Funding

Asthma Positional Candidate Genes in Mice and HumansR01HL067736 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLS-KARP, MARSHA · 2000 to 2010
$4.1M
APPLIED GENOMICS IN CARDIOPULMONARY DISEASEU01HL066623 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SCOTT, ALAN L · 2000 to 2003
$3.1M
Complement in Allergic Asthma: The role of C3a and C5aR01AI057839 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI KOEHL, JOERG · 2004 to 2008
$1.8M
DYSREGULATION OF IL12 IN ALLERGIC INFLAMMATIONR01HL058527 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI WILLS-KARP, MARSHA W · 1997 to 2000
$234k
NHLBI NIH HHS HL58527NHLBI NIH HHS HL66623NHLBI NIH HHS HL67736NIAID NIH HHS AI057839
6 · The paper itself

Abstract

Despite extensive inquiry, the mechanisms underlying the pathophysiology of allergic diseases remain unknown. Recently, there has been a resurgence of interest in the role of the innate immune mediators of the complement pathway in asthma pathogenesis, particularly the anaphylatoxins (C3a, C5a). The emerging paradigm is that C3a production at the airway surface serves as a common pathway for the induction of airway hyperresponsiveness to a variety of asthma triggers (ie, allergens, viral infections, particulate matter, ozone, smoke), whereas C5/C5a plays a dual immunoregulatory role by protecting against Th2-mediated immune responses during initiation of responses and a proinflammatory role once immune responses are established. Support for a causal role for altered anaphylatoxin production in human disease comes from reports of exaggerated complement production in the lungs of asthmatics as well as the association of asthma with polymorphisms in C3/C3aR genes. Herein, we explore our current understanding of the role of complement activation in asthma pathogenesis and highlight the potential of targeting complement pathways for therapeutic drug development.

Indexed as

Complement ActivationAnimalsAsthmaGenetic Predisposition to DiseaseHumansHypersensitivity

Identifiers

PMID16091207
OpenAlexW1982434943

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.