Molecular and Cellular Mechanisms of Type 1 Diabetes (T1D)

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1603

Special Issue Editors


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Guest Editor
College of Medicine, University of Florida, Gainesville, FL, USA
Interests: autoimmunity; inflammation; genetic mutations; single nucleotide polymorphisms (SNPs); T cell biology; innate immunity; cell signaling; viral/bacterial triggers

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Guest Editor
Diabetes Unit, The Faculty of Medicine, Department of Endocrinology and Metabolism, Hadassah Medical Center, Hebrew University of Jerusalem, Jerusalem 91120, Israel
Interests: insulin resistance; diabetes; lipid metabolism; glucose metabolism; disease prevention; obesity metabolic endocrinology; high fructose corn syrup; cardiovascular disease; obesity; telemedicine; telehealth; eHealth; mHealth; digital health; review; connected diabetes care; diabetes mellitus; glucose monitoring
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Special Issue Information

Dear Colleagues,

Type 1 diabetes (T1D) is an extremely complex disease, where pathogenesis is highly debated. Many different genetic meta-analyses and full-genome sequencing have divulged a wide range of genetic risk factors, where single-nucleotide polymorphisms (SNPs) and other anomalies have been associated with the disease. However, many of these mutations have not been properly connected towards how precisely they contribute to pancreatic beta cell destruction on a molecular or cellular level. It is also unclear how exactly environmental pressures and pathogens contribute as triggers of an autoimmune response towards beta cells. The connection between both genetic and environmental triggers towards T1D development needs to be better identified and how on a mechanistic level do these two factors lead towards pancreatic cellular destruction. 

Some questions that will be answered in this Special Issue include the following: How do SNPs involved with immunoregulatory genes and even non-immunoregulatory genes affect the way immune cells process antigens and allow autoantigens to elicit an immune response towards oneself? Do pathogens and other environmental factors trigger these SNPs to cause an autoimmune response? Why are pancreatic beta cells targeted specifically in T1D development? What other risk factors are involved in an autoimmune response on the molecular and cellular level? 

These and many more questions will be the focus of this Special Issue, where it will highlight recent findings on how both the genetic and environmental factors contribute towards T1D and how do they contribute towards targeting pancreatic beta cells on a cellular level. The overall goal of this Issue is to provide researchers with research papers, reviews, and meta-analyses concentrated on identifying key genes and other triggers that lead to the development of T1D, focusing on molecular and cellular techniques. 

Dr. Robert Sharp
Prof. Dr. Itamar Raz
Guest Editors

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Keywords

  • T1D
  • autoimmunity
  • type 1 diabetes
  • single-nucleotide polymorphisms (SNPs)
  • viral/bacterial pathogens
  • T-cell biology
  • inflammation
  • pancreatic beta cells
  • immunoregulatory
  • molecular biology
  • cellular biology

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Published Papers (1 paper)

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Research

20 pages, 472 KB  
Article
Clinical Characterization of Atypical Diabetes: Insights from the GENEPEDIAB Study into the Spectrum Between Type 1 and Monogenic Diabetes
by Antoine Harvengt, Gauthier Pirlot, Leyan Denizli, Zain Syed, Sophie Welsch, Dominique Beckers, Thierry Mouraux, Nicole Seret, Marie-Christine Lebrethon, Raphael Helaers, Pascal Brouillard, Miikka Vikkula and Philippe A. Lysy
Cells 2026, 15(5), 484; https://doi.org/10.3390/cells15050484 - 7 Mar 2026
Viewed by 945
Abstract
Background: Type 1 diabetes (T1D) shares clinical characteristics with other forms of diabetes, particularly monogenic diabetes such as maturity-onset diabetes of the young (MODY). Differential diagnosis is complicated by the existence of intermediate phenotypes. We aimed to delineate the phenotypic continuum between T1D [...] Read more.
Background: Type 1 diabetes (T1D) shares clinical characteristics with other forms of diabetes, particularly monogenic diabetes such as maturity-onset diabetes of the young (MODY). Differential diagnosis is complicated by the existence of intermediate phenotypes. We aimed to delineate the phenotypic continuum between T1D and monogenic diabetes. Methods: The multicentric GENEPEDIAB study included patients aged 6 months to 18 years diagnosed with diabetes and treated for either T1D or monogenic diabetes. Analyses comprised glycemic variability, continuous glucose monitoring metrics, application of the DIAMODIA criteria, and genetic investigations. Results: A gradient was observed across T1D, atypical diabetes (Adia), and MODY cohorts for several glycemic parameters. T1D patients exhibited values furthest from treatment targets, whereas MODY patients showed better glycemic control. Stratification of the Adia cohort according to the number of positive DIAMODIA criteria further supported this trend, as demonstrated by glycemic measures and multiple correspondence analysis. Genetic analyses did not identify a uniform causative variant in the Adia cohort; however, several rare variants, including variants of uncertain significance and likely pathogenic variants in diabetes-related genes, were detected. Conclusions: These findings showed, in our specific cohort of pediatric patients, the existence of a phenotypic gradient between T1D and monogenic diabetes, with atypical diabetes occupying an intermediate position, including when stratified by DIAMODIA criteria. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Type 1 Diabetes (T1D))
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