Evidence map›Paper›PMID 19895849›Full record

ReviewImmunology letters2010

Regulation of human mast cell and basophil function by anaphylatoxins C3a and C5a.

Hydar Ali

Abstract readReview
In one paragraph

Review in Immunology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

56 citing papers in PubMed, 114 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Observational
  8. Article
  9. Review
  10. Article
  11. Mast Cells in Autism Spectrum Disorder-The Enigma to Be Solved?International journal of molecular sciences · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Allergy, Anaphylaxis, and Nonallergic Hypersensitivity: IgE, Mast Cells, and Beyond.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2022
    Review
  20. 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.

Hydar AliDepartment of Pathology, University of Pennsylvania School of Dental Medicine, 240 South 40th Street, Philadelphia, PA 19104-6030, USA. alih@upenn.edu
University of Pennsylvania · US

Funding

G Protein Coupled Receptor Signaling in Mast CellsR01HL085774 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ALI, HYDAR · 2008 to 2011
$1.6M
G-PROTEIN COUPLED RECEPTORS IN ASTHMA AND INFLAMMATIONR01HL063372 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ALI, HYDAR · 2000 to 2003
$1.1M
NHLBI NIH HHS HL063372NHLBI NIH HHS HL085774NHLBI NIH HHS R01 HL063372NHLBI NIH HHS R01 HL085774
6 · The paper itself

Abstract

Allergic diseases such as asthma result from inappropriate immunologic responses to common environmental allergens in genetically susceptible individuals. Following allergen exposure, interaction of dendritic cells (DC) with CD4(+) T cells leads to the production of Th2 cytokines, which induce B cells to synthesize IgE molecules (sensitization phase). These IgE molecules bind to their high affinity receptors (FcvarepsilonRI) on the surface of mast cells and basophils and their subsequent cross-linking by allergen results in the release of preformed and newly synthesized mediators, which cause bronchoconstriction, lung inflammation and airway hyperresponsiveness (AHR) in asthma (effector phase). The complement components C3a and C5a levels are increased in the lungs of patients with asthma and are likely generated via the actions of both allergen and mast cell proteases. In vivo studies with rodents have shown that while C3a facilitates allergen sensitization in some models C5a inhibits this response. Despite this difference, both anaphylatoxins promote lung inflammation and AHR in vivo indicating that cells other than DC and T cells likely mediate the functional effects of C3a and C5a in asthma. This review focuses on the contribution of C3a and C5a in the pathogenesis of asthma with a particular emphasis on mast cells and basophils. It discusses the mechanisms by which anaphylatoxins activate mast cells and basophils and the associated signaling pathways via which their receptors are regulated by priming and desensitization.

Indexed as

AnimalsAsthmaBasophilsCell DegranulationComplement C3aComplement C5aDesensitization, ImmunologicHumansInflammationLungMast CellsMiceRatsReceptors, G-Protein-CoupledSignal TransductionComplement C3aComplement C5aReceptors, G-Protein-Coupled

Identifiers

PMID19895849
PMCPMC2815128
OpenAlexW2065139897

What OpenQuestion holds

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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.