Nfkbid Overexpression in Nonobese Diabetic Mice Elicits Complete Type 1 Diabetes Resistance in Part Associated with Enhanced Thymic Deletion of Pathogenic CD8 T Cells and Increased Numbers and Activity of Regulatory T Cells.
Journal of immunology (Baltimore, Md. : 1950)
JMG, Animals, CD8-Positive T-Lymphocytes, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 1, Humans, Mice, Mice, Inbred NOD, Mice, Transgenic, T-Lymphocytes, Regulatory
J Immunol 2022 Jul 15; 209(2):227-237
Type 1 diabetes (T1D) in both humans and NOD mice is caused by T cell-mediated autoimmune destruction of pancreatic β cells. Increased frequency or activity of autoreactive T cells and failures of regulatory T cells (Tregs) to control these pathogenic effectors have both been implicated in T1D etiology. Due to the expression of MHC class I molecules on β cells, CD8 T cells represent the ultimate effector population mediating T1D. Developing autoreactive CD8 T cells normally undergo extensive thymic negative selection, but this process is impaired in NOD mice and also likely T1D patients. Previous studies identified an allelic variant of
Nfkbid Overexpression in Nonobese Diabetic Mice Elicits Complete Type 1 Diabetes Resistance in Part Associated with Enhanced Thymic Deletion of Pathogenic CD8 T Cells and Increased Numbers and Activity of Regulatory T Cells. J Immunol 2022 Jul 15; 209(2):227-237
We thank the staff at The Jackson Laboratory’s Flow Cytometry service, Research Animal Facility, Genetic Engineering Technologies, and Genome Technology groups for technical support. We thank the National Institutes of Health Tetramer Facility for providing AI4 tetramer. We are also grateful for a generous donation from Carl Stewie and his wife, Maike Rohde, toward T1D research at The Jackson Laboratory.