Evidence map›Paper›PMID 26410782›Full record

ArticleThe Journal of allergy and clinical immunology2016

IgE antibodies, FcεRIα, and IgE-mediated local anaphylaxis can limit snake venom toxicity.

Philipp Starkl, Thomas Marichal, Nicolas Gaudenzio, Laurent Lionel Reber, Riccardo Sibilano, Mindy Tsai, Stephen Joseph Galli

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  5. Article
  6. Whence and wherefore IgE?Immunological reviews · 2024
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  13. Mast cell-derived BH4 is a critical mediator of postoperative pain.bioRxiv : the preprint server for biology · 2023
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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

7 authors at 1 institution in 1 country.

Philipp StarklDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif.
Thomas MarichalDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif.
Nicolas GaudenzioDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif.
Laurent Lionel ReberDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif.
Riccardo SibilanoDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif.
Mindy TsaiDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif.
Stephen Joseph GalliDepartment of Pathology, Stanford University School of Medicine, Stanford, Calif; Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, Calif. Electronic address: sgalli@stanford.edu.
Stanford University · US

Funding

Spectrum Stanford Center for clinical and Translational Research and EducationUL1TR001085 · NCATS · STANFORD UNIVERSITY · PI CULLEN, MARK RICHARD, GREENBERG, HARRY BERNARD · 2013 to 2017
$37.1M
Stanford Center for Clinical and Translational Education and Research (SCCTER)UL1UL1RR025744 · NCRR · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 2008 to 2011
$22.4M
Role of Mast Cells in Inflammation and ImmunityR01CA072074 · NCI · STANFORD UNIVERSITY · PI GALLI, STEPHEN JOSEPH · 1996 to 2010
$4.4M
Expression and Modulation of Mast Cell Function in AsthmaR01AI070813 · NIAID · STANFORD UNIVERSITY · PI GALLI, STEPHEN JOSEPH · 2006 to 2010
$2.5M
Regulation of Mast Cell Development and FunctionR01AI023990 · NIAID · STANFORD UNIVERSITY · PI GALLI, STEPHEN JOSEPH · 1986 to 2010
$2.4M
REGULATION OF MAST CELL DEVELOPMENT &FUNCTIONR37AI023990 · NIAID · STANFORD UNIVERSITY · PI GALLI, STEPHEN J · 1996 to 2005
$2.2M
Neutrophils as therapeutic targets in cryopyrin-associated periodic syndromeK99AI110645 · NIAID · STANFORD UNIVERSITY · PI REBER, LAURENT LIONEL · 2014 to 2014
$130k
NCATS NIH HHS UL1 TR001085NCI NIH HHS CA072074NCI NIH HHS R01 CA072074NCRR NIH HHS UL1 RR025744NIAID NIH HHS AI023990NIAID NIH HHS AI070813NIAID NIH HHS K99 AI110645NIAID NIH HHS K99AI110645NIAID NIH HHS R01 AI023990NIAID NIH HHS R01 AI070813NIAID NIH HHS R37 AI023990
6 · The paper itself

Abstract

backgroundType 2 cytokine-related immune responses associated with development of antigen-specific IgE antibodies can contribute to pathology in patients with allergic diseases and to fatal anaphylaxis. However, recent findings in mice indicate that IgE also can enhance defense against honeybee venom.

objectiveWe tested whether IgE antibodies, IgE-dependent effector mechanisms, and a local anaphylactic reaction to an unrelated antigen can enhance defense against Russell viper venom (RVV) and determined whether such responses can be influenced by immunization protocol or mouse strain.

methodsWe compared the resistance of RVV-immunized wild-type, IgE-deficient, and Fcer1a-deficient mice after injection of a potentially lethal dose of RVV.

resultsA single prior exposure to RVV enhanced the ability of wild-type mice, but not mice lacking IgE or functional FcεRI, to survive challenge with a potentially lethal amount of RVV. Moreover, IgE-dependent local passive cutaneous anaphylaxis in response to challenge with an antigen not naturally present in RVV significantly enhanced resistance to the venom. Finally, we observed different effects on resistance to RVV or honeybee venom in BALB/c versus C57BL/6 mice that had received a second exposure to that venom before challenge with a high dose of that venom.

conclusionThese observations illustrate the potential benefit of IgE-dependent effector mechanisms in acquired host defense against venoms. The extent to which type 2 immune responses against venoms can decrease pathology associated with envenomation seems to be influenced by the type of venom, the frequency of venom exposure, and the genetic background of the host.

Indexed as

AnaphylaxisAnimalsBee VenomsCell DegranulationFemaleImmunizationImmunoglobulin EMast CellsMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicReceptors, IgEViper VenomsBee VenomsFcepsilonRIalpha protein, mouseImmunoglobulin EReceptors, IgEViper VenomsAcquired resistanceallergyDaboia russeliiFcεRIαhoneybeeIgEmast cellsRussell vipertoxin hypothesistype 2 immunityvenom

Identifiers

PMID26410782
PMCPMC4715494
OpenAlexW1790300783

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.