Host gene effects on gut microbiota in type 1 diabetes
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Updated: Sep 24, 2025

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
Keyu Guo1, Juan Huang1,2, Zhiguang Zhou1
1National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology (Central South University), Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Abstract:
Type 1 diabetes (T1D) is an organ-specific autoimmune disease characterized by progressive pancreatic β-cell loss. Both a predisposing genetic background, that may encompass mutations in several genes, as well as exposure to environmental factors can affect the progression of autoimmune responses to multiple pancreatic islet autoantigens. Many genetic variants that increase the risk of T1D are found in immunity genes involved in sensing and responding to microorganisms. Although increasing evidence indicates that the gut microbiome composition may promote or prevent T1D development, little is known about the link between gut microbiota and T1D susceptibility genes in patients with T1D. Recent studies in the inbred non-obese diabetic (NOD) mouse, a widely used model of T1D, have suggested that many genetic loci can influence gut microbiome composition to modulate islet autoimmunity. This review summarizes evidence that examines the effect of host genes on gut microbiota diversity and function during T1D development. Knowledge of the host gene-gut microbiota interactions at play during T1D progression may help us identify new diagnostic and prognostic tools and help also design effective strategies for disease treatment.
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