Effect of X‐ and Y‐Box Deletions on the Development of Diabetes in H‐2Eα‐Chain Transgenic Nonobese Diabetic Mice
Explore this paper's citation graph
Summary
Transgenic NOD mice constructed where the X and Y boxes of the Ead gene have been functionally deleted are constructed, and NOD ΔY1 animals are protected from diabetes development, while ΔX mice remain susceptible, albeit to a lesser extent than the parental NOD strain.
- Type
- article
- Published
- 2006-01-01
- Cited by
- 2
- References
- 32
- Access
- Open access
- OpenAlex
- https://openalex.org/W1984596326
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:23649035
Keywords
Nod, NOD mice, Transgene, Genetically modified mouse, Major histocompatibility complex
References
- The effect of bone marrow and thymus chimerism between non‐obese diabetic (NOD) and NOD‐E transgenic mice, on the expression and prevention of diabetes
- Quantitative thresholds of MHC class II I-E expressed on hemopoietically derived antigen-presenting cells in transgenic NOD/Lt mice determine level of diabetes resistance and indicate mechanism of protection.
- Aspartate at position 57 of nonobese diabetic I-Ag7 beta-chain diminishes the spontaneous incidence of insulin-dependent diabetes mellitus.
- IL-12 Administration Reveals Diabetogenic T Cells in Genetically Resistant I-Eα-Transgenic Nonobese Diabetic Mice: Resistance to Autoimmune Diabetes Is Associated with Binding of Eα-Derived Peptides to the I-Ag7 Molecule1
- Restriction fragment length polymorphisms in the major histocompatibility complex of the non-obese diabetic mouse.
- Inhibition of Autoimmune Diabetes in Nonobese Diabetic Mice by Transgenic Restoration of H2-E MHC Class II Expression: Additive, But Unequal, Involvement of Multiple APC Subtypes1
- Genetic control of diabetes and insulitis in the nonobese diabetic mouse. Pedigree analysis of a diabetic H-2nod/b heterozygote.
- Breeding of a non-obese, diabetic strain of mice.
- Characterization of pancreatic islet cell infiltrates in NOD mice: effect of cell transfer and transgene expression
- E expression is needed on both bone marrow derived cells and thymic epithelium to increase IL-4 production and achieve protection in NOD bone marrow chimeras.
- The NOD mouse: recessive diabetogenic gene in the major histocompatibility complex.
- Immune disturbance and pathogenesis of non-obese diabetes-prone (NOD) mice.
- Conserved major histocompatibility complex class II boxes--X and Y--are transcriptional control elements and specifically bind nuclear proteins.
- Prevention of autoimmune insulitis by expression of I–E molecules in NOD mice
- MHC-linked protection from diabetes dissociated from clonal deletion of T cells.
- A technique for radiolabeling DNA restriction endonuclease fragments to high specific activity.
- The complete nucleotide sequence of the I-E alpha d immune response gene.
- Direct evidence for the contribution of the unique I-ANOD to the development of insulitis in non-obese diabetic mice
- Prevention of insulin-dependent diabetes mellitus in non-obese diabetic mice by transgenes encoding modified I-A β-chain or normal I-E α-chain
- The first external domain of the nonobese diabetic mouse class II I-A beta chain is unique.
Cited by
Related papers
- Studies on the thymus of non-obese diabetic (NOD) mice: effect of transgene expression.
- Elevated glucagon-like peptide-1 plasma levels, as a possible adaptive response, in diabetic NOD mice.
- Direct evidence for the contribution of B cells to the progression of insulitis and the development of diabetes in non-obese diabetic mice.
- I-E+ nonobese diabetic mice develop insulitis and diabetes
- Altered autoimmune response in NOD-Alox15null mice
- Postnatal Hematopoiesis and Gut Microbiota in NOD Mice Deviate from C57BL/6 Mice
- Effect of the expression of DR alpha E beta NOD molecule on the development of insulitis and diabetes in the non-obese diabetic (NOD) mouse.
- Both central and peripheral tolerance mechanisms play roles in diabetes prevention in NOD-E transgenic mice
- Pig islet xenografts are resistant to autoimmune destruction by non‐obese diabetic recipients after anti‐CD4 treatment