Evidence map›Paper›PMID 30645205›Full record

ArticleThe Journal of clinical investigation2019

CD33 recruitment inhibits IgE-mediated anaphylaxis and desensitizes mast cells to allergen.

Shiteng Duan, Cynthia J Koziol-White, William F Jester, Scott A Smith, Corwin M Nycholat, Matthew S Macauley, Reynold A Panettieri, James C Paulson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
8.5field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Emerging Therapies for Anaphylaxis.Immunology and allergy clinics of North America · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Exploring Siglecs: Potential Modulators of Immune Cells in Food Allergy and Therapeutic Applications.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025
    Review
  7. Article
  8. Review
  9. Induced proximity at the cell surface.Nature biotechnology · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Siglec-9 is an inhibitory receptor on human mast cells in vitro.The Journal of allergy and clinical immunology · 2023
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Shiteng DuanDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
Cynthia J Koziol-WhiteRutgers Institute for Translational Medicine and Science, Rutgers University, New Brunswick, New Hampshire, USA.
William F JesterRutgers Institute for Translational Medicine and Science, Rutgers University, New Brunswick, New Hampshire, USA.
Scott A SmithDepartment of Medicine, and Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Vanderbilt University, Nashville, Tennessee, USA
Corwin M NycholatDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
Matthew S MacauleyDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
Reynold A PanettieriRutgers Institute for Translational Medicine and Science, Rutgers University, New Brunswick, New Hampshire, USA.
James C PaulsonDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.
Scripps Research Institute · USRutgers, The State University of New Jersey · US

Funding

Treating lung inflammation by targeting SiglecsP01HL107151 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SCHNAAR, RONALD L · 2011 to 2017
$15.4M
Using siglecs and their ligands to treat allergic diseases SALTADU19AI136443 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHNAAR, RONALD L · 2018 to 2022
$7.6M
Exploiting inhibitory Siglecs for desensitizing mast cellsR01AI132790 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI PAULSON, JAMES C · 2018 to 2022
$3.1M
Inducing antigen specific B cell toleranceR01AI099141 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI PAULSON, JAMES C · 2012 to 2016
$2.3M
NHLBI NIH HHS P01 HL107151NIAID NIH HHS R01 AI099141NIAID NIH HHS R01 AI132790NIAID NIH HHS U19 AI136443
6 · The paper itself

Abstract

Allergen immunotherapy for patients with allergies begins with weekly escalating doses of allergen under medical supervision to monitor and treat IgE mast cell-mediated anaphylaxis. There is currently no treatment to safely desensitize mast cells to enable robust allergen immunotherapy with therapeutic levels of allergen. Here, we demonstrated that liposomal nanoparticles bearing an allergen and a high-affinity glycan ligand of the inhibitory receptor CD33 profoundly suppressed IgE-mediated activation of mast cells, prevented anaphylaxis in Tg mice with mast cells expressing human CD33, and desensitized mice to subsequent allergen challenge for several days. We showed that high levels of CD33 were consistently expressed on human skin mast cells and that the antigenic liposomes with CD33 ligand prevented IgE-mediated bronchoconstriction in slices of human lung. The results demonstrated the potential of exploiting CD33 to desensitize mast cells to provide a therapeutic window for administering allergen immunotherapy without triggering anaphylaxis.

Indexed as

Desensitization, ImmunologicAllergensAnaphylaxisAnimalsBronchoconstrictionHumansImmunoglobulin EMast CellsMiceMice, TransgenicSialic Acid Binding Ig-like Lectin 3AllergensCD33 protein, humanCd33 protein, mouseImmunoglobulin ESialic Acid Binding Ig-like Lectin 3GlycobiologyImmunologyMast cellsNanotechnologyTherapeutics

Identifiers

PMID30645205
PMCPMC6391081
OpenAlexW2909993605

What Socratic 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 Socratic graph.