Evidence map›Paper›PMID 24056872›Full record

ArticleMolecular bioSystems2013

An IgE receptor mimetic peptide (PepE) protects mice from IgE mediated anaphylaxis.

Joseph S Zhou, Annamaria Sandomenico, Valeria Severino, Oliver T Burton, Alanna Darling, Hans C Oettgen, Menotti Ruvo

Abstract read
In one paragraph

Article in Molecular bioSystems, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Inhibition of three novel Radix Scutellariae extracts on immediate hypersensitivity.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2014
    Article
  8. IgE induces proliferation in human airway smooth muscle cells: role of MAPK and STAT3 pathways.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2013
    Article
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.

Joseph S ZhouBoston Children's Hospital, Boston, MA 02115, USA. Hans.Oettgen@childrens.harvard.edu.
Annamaria Sandomenico
Valeria Severino
Oliver T Burton
Alanna Darling
Hans C Oettgen
Menotti Ruvo

Funding

MOLECULAR BASIS OF ALLERGIC AND IMMUNOLOGIC DISEASET32AI007512 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI Janet Chou, Peter A Nigrovic · 1996 to 2026
$13.1M
Role of IL-4R-alpha signaling in food allergen sensitization and anaphylaxisR56AI100889 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI OETTGEN, HANS C · 2012 to 2012
$290k
NIAID NIH HHS R56 AI100889NIAID NIH HHS R56 AI100889-01NIAID NIH HHS T32 AI007512NIAID NIH HHS T32AI007512
6 · The paper itself

Abstract

Crosslinking of receptor-bound Immunoglobulin E (IgE) triggers immediate hypersensitivity reactions including anaphylaxis. Blocking the interaction of IgE with its high-affinity receptor, FcεRI, on mast cells and basophils is an attractive strategy for the treatment of allergies. This approach has seen clinical success using the anti-IgE monoclonal antibody, omalizumab. We recently designed and characterized a novel FcεRI-mimetic peptide (PepE) which contains the two key FcεRI α-chain receptor loops known to interact with the ε-heavy chain of IgE, C'-E and B-C, with an optimized linker for joining them. PepE has high specificity and affinity for IgE, blocks IgE binding to FcεRI and prevents IgE-induced mediator release from RBL2H3 cells. We have now investigated the biological effects of this peptide in vivo using a line of mice (BALB/c Il4raF709) very sensitive to IgE-mediated systemic anaphylaxis. IgE-deficient (IgE-/-) Il4raF709 mice were passively sensitized with the anti-DNP IgE monoclonal antibody (SPE-7) and subsequently challenged i.v. with DNP-BSA. Mice receiving a single dose of PepE prior to sensitization with SPE-7 IgE were fully protected from anaphylaxis while vehicle control-treated mice displayed strong reactions with significant core body temperature drops and elevated levels of mouse mast cell protease-1 (mMCP-1) in the serum. However, PepE had no effect on IgE-mediated anaphylaxis if given after IgE administration in IgE-/- mice, suggesting that PepE can block binding of free IgE to FcεRI but cannot compete with the receptor for already bound IgE in vivo. A single dose of PepE treatment did not protect IgE sufficient mice from IgE mediated anaphylaxis. However, a 3 week long course of PepE treatment protected IgE sufficient Il4raF709 mice from body temperature drops and elevation of serum mMCP-1. Our findings establish the potential of this type of structure for blocking IgE binding to mast cells in vivo and suggest that related peptides might have the potential to attenuate clinical allergic reactions.

Indexed as

Molecular MimicryAmino Acid SequenceAnaphylaxisAnimalsDisease Models, AnimalFemaleImmunoglobulin EMiceMice, KnockoutPeptidesProtein BindingReceptors, IgETime FactorsImmunoglobulin EPeptidesReceptors, IgE

Identifiers

PMID24056872
PMCPMC3820499

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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.