Evidence map›Paper›PMID 32679754›Full record

ReviewNutrients2020

Gluten Degrading Enzymes for Treatment of Celiac Disease.

Guoxian Wei, Eva J Helmerhorst, Ghassan Darwish, Gabriel Blumenkranz, Detlef Schuppan

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Novel probiotic preparation withMicrobiology spectrum · 2024
    Trial
  3. Effect ofWorld journal of gastroenterology · 2024
    Trial
  4. Review
  5. Harnessing gut microbiome enzymes:Microbiology spectrum · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Recent Advances in Gluten-Related Disorders.International journal of molecular sciences · 2025
    Article
  17. Celiac Disease: Beyond Diet and Food Awareness.Foods (Basel, Switzerland) · 2025
    Review
  18. Review
  19. Article
  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

5 authors at 1 institution in 2 countries.

Guoxian WeiDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, 700 Albany Street, Boston, MA 02118, USA.ORCID 0000-0001-5115-3697
Eva J HelmerhorstDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, 700 Albany Street, Boston, MA 02118, USA.
Ghassan DarwishDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, 700 Albany Street, Boston, MA 02118, USA.
Gabriel BlumenkranzDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, 700 Albany Street, Boston, MA 02118, USA.
Detlef SchuppanInstitute for Translational Immunology and Research Center for Immunotherapy (FZI), Johannes Gutenberg University (JGU) Medical Center, 55131 Mainz, Germany.
Beth Israel Deaconess Medical Center · US

Funding

German Research Foundation DFG Schu 646/17-1 (wheat and ATI), DFG Schu 646/20-1 (Allergy), DFG Pic/Schu SPP1656 (Intestinal microbiota)NIH HHS R01 AI087803 (EJH), K02 AI101067 (EJH)The Leibniz Foundation SAW-2016-DFA-2 (Wheatscan)
6 · The paper itself

Abstract

Celiac disease (CeD) affects about 1% of most world populations. It presents a wide spectrum of clinical manifestations, ranging from minor symptoms to mild or severe malabsorption, and it may be associated with a wide variety of autoimmune diseases. CeD is triggered and maintained by the ingestion of gluten proteins from wheat and related grains. Gluten peptides that resist gastrointestinal digestion are antigenically presented to gluten specific T cells in the intestinal mucosa via HLA-DQ2 or HLA-DQ8, the necessary genetic predisposition for CeD. To date, there is no effective or approved treatment for CeD other than a strict adherence to a gluten-free diet, which is difficult to maintain in professional or social environments. Moreover, many patients with CeD have active disease despite diet adherence due to a high sensitivity to traces of gluten. Therefore, safe pharmacological treatments that complement the gluten-free diet are urgently needed. Oral enzyme therapy, employing gluten-degrading enzymes, is a promising therapeutic approach. A prerequisite is that such enzymes are active under gastro-duodenal conditions, quickly neutralize the T cell activating gluten peptides and are safe for human consumption. Several enzymes including prolyl endopeptidases, cysteine proteases and subtilisins can cleave the human digestion-resistant gluten peptides in vitro and in vivo. Examples are several prolyl endopeptidases from bacterial sources, subtilisins from

Indexed as

AutoimmunityCeliac DiseaseDiet, Gluten-FreeDrug CompoundingEnzyme StabilityFemaleGenetic Predisposition to DiseaseGlutensHLA-DQ AntigensHumansMaleProlyl OligopeptidasesProteolysisSubtilisinsT-LymphocytesGlutensHLA-DQ2 antigenHLA-DQ8 antigenHLA-DQ AntigensProlyl OligopeptidasesSubtilisinsautoimmunityceliac diseaseendopeptidaseenteric coatingenzyme therapyglutenglutenasetreatmentwheat

Identifiers

PMID32679754
PMCPMC7400306
OpenAlexW3042554898

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.