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Molecular Mechanisms, Emerging Biomarkers, Novel Therapies and Personalized Treatment in Celiac Disease (CD)

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 April 2026 | Viewed by 2049

Special Issue Editor

Dr. María Isabel Torres

E-Mail Website
Guest Editor
Department of Experimental Biology, Faculty of Health Sciences, University of Jaén, 23071 Jaén, Spain
Interests: celiac disease; intestinal organoids; extracellular microvesicles in liquid biopsy; immune checkpoints
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Understanding the molecular mechanisms of CD, coupled with the development of new biomarkers and therapies, are contributting for more effective and personalized management of the disease. Advances in research continue to hold promise for improving the quality of life for individuals affected by celiac disease. Emerging biomarkers are being developed to improve the diagnosis and management of CD. These include deamidated gliadin peptides (DGPs), cytokine profiles, microRNAs, and markers of intestinal permeability. Microbial biomarkers and specific proteins found in blood and stool are also being explored for their potential to enhance diagnostic accuracy and monitor disease activity. In terms of novel therapies, there is ongoing research aimed at developing treatments that go beyond the traditional gluten-free diet (GFD). Some strategies include enzyme therapies to break down gluten, gluten-sequestering agents, inhibitors of TG2 to prevent the immune response, and therapies to modulate intestinal permeability and the gut microbiome. Additionally, nanoparticle-based delivery systems and genetic and cell-based therapies, such as gene editing and adoptive cell transfer, are being investigated for their potential to offer more personalized and effective treatment options. These advancements hold promise for improving the quality of life for individuals with CD by providing more precise diagnostic tools, better monitoring capabilities, and potentially curative treatments.

Thus, this Special Issue entitled ‘Molecular Mechanisms, Emerging Biomarkers, Novel Therapies and Personalized Treatment in Celiac Disease (CD) will explores recent advancements in understanding and managing CD.

Dr. María Isabel Torres
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • celiac disease
  • gluten sensitivity
  • immune response
  • emerging biomarkers
  • novel therapies
  • microbiome modulation
  • personalized treatment

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Published Papers (2 papers)

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Research

16 pages, 1649 KB  
Article
Standardizing Intestinal Permeability Assessment: Optimization of Gluten Dose and Urine Collection Times for u-GIP and Lactulose:Mannitol Ratio in Healthy Volunteers
by Raquel Rodríguez-Ramírez, María Auxiliadora Fernández Peralbo, Ángel Cebolla and Carolina Sousa
Int. J. Mol. Sci. 2026, 27(5), 2286; https://doi.org/10.3390/ijms27052286 - 28 Feb 2026
Viewed by 257
Abstract
Urinary gluten immunogenic peptides (u-GIPs) have been proposed as a complementary marker to classical intestinal permeability tests based on lactulose, mannitol, and the lactulose:mannitol ratio (LMR). However, the effects of gluten dose, urine collection interval, and sampling strategy on their performance remain insufficiently [...] Read more.
Urinary gluten immunogenic peptides (u-GIPs) have been proposed as a complementary marker to classical intestinal permeability tests based on lactulose, mannitol, and the lactulose:mannitol ratio (LMR). However, the effects of gluten dose, urine collection interval, and sampling strategy on their performance remain insufficiently defined. This study evaluated these variables to support protocol standardization. Data from four standardized protocols including 46 healthy adults exposed to 0, 2, 4, or 10 g of gluten were analyzed. All participants ingested fixed doses of lactulose and mannitol. Urine was collected cumulatively (0–6 h and 0–15 h) or by individual voids. u-GIP levels were measured by lateral-flow immunoassay, and lactulose and mannitol by ion chromatography. u-GIP excretion showed a clear dose dependence. Lactulose excretion increased transiently only at the 10 g dose during the 0–6 h interval, while mannitol excretion and LMR were unaffected. The u-GIP excretion index showed linear proportionality at the 2 g and 4 g doses but exhibited saturation kinetics at the 10 g dose. The 4 g dose showed the lowest interindividual variability. Sampling strategies yielded equivalent results. A 4 g gluten challenge combined with a 6 h urine collection demonstrated effectiveness in healthy volunteers and may be suitable for clinical application. Further research involving larger cohorts of both healthy individuals and patients with intestinal hyperpermeability is required to validate this method. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Emerging Biomarkers, Novel Therapies and Personalized Treatment in Celiac Disease (CD))
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64 pages, 8019 KB  
Article
BTN2A1 and BTN3A1 as Novel Coeliac Disease Risk Loci: An In Silico Analysis
by Kim Ngan Luu Hoang, Shelley Evans, Thomas W. Willis, Kate Davies, Hannah Kockelbergh, Lee Silcock, Kim Piechocki, Anna Fowler and Elizabeth J. Soilleux
Int. J. Mol. Sci. 2025, 26(21), 10697; https://doi.org/10.3390/ijms262110697 - 3 Nov 2025
Cited by 2 | Viewed by 1154
Abstract
Coeliac disease (CeD) is a gastrointestinal enteropathy triggered by the consumption of gluten in predisposed individuals. A recent study showed that individuals were at more than 10% risk of having CeD if a first-degree relative also had the disease. However, only around 50% [...] Read more.
Coeliac disease (CeD) is a gastrointestinal enteropathy triggered by the consumption of gluten in predisposed individuals. A recent study showed that individuals were at more than 10% risk of having CeD if a first-degree relative also had the disease. However, only around 50% of CeD genetic heritability is attributable to specific loci, with the majority of this heritable risk attributed to the HLA loci, while the remaining 50% of disease risk is currently unidentified. We investigated the butyrophilin family of immunomodulators as novel CeD risk loci. We sequenced the butyrophilin loci of 48 CeD and 46 control patients and carried out gene-based burden testing on the captured single-nucleotide polymorphisms (SNPs). We found a significantly increased BTN2A1 gene burden in CeD patients. To validate these results, the SNP data of 3094 CeD patients and 29,762 control participants from the UK Biobank database were subjected to single-variant analyses. Fourteen BTN2A1, ten BTN3A1, and thirteen BTN3A2 SNPs were significantly associated with CeD status. These results are interesting, as BTN2A1 and BTN3A2 have not been associated with CeD risk previously but are known to modulate the activation of Vγ9+ γδ T cells and NK cells. Twenty of the 37 SNPs above were associated with CeD status independent of the risk-associated HLA genotypes. All twenty of these SNPs, alongside a novel SNP not included in the above SNPs, were associated with CeD in HLA-DQ2.5-matched case-control groups. We reaffirm the association of the BTN3A2 locus with CeD risk and identify BTN2A1 and BTN3A1 as putative novel CeD risk loci. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Emerging Biomarkers, Novel Therapies and Personalized Treatment in Celiac Disease (CD))
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