His primary areas of investigation include Nod, Endocrinology, Internal medicine, NOD mice and Immunology. Edward H. Leiter combines subjects such as Congenic, Severe combined immunodeficiency, Major histocompatibility complex and Locus with his study of Nod. His work on Lipid metabolism as part of general Internal medicine study is frequently linked to Metabolome, bridging the gap between disciplines.
His research integrates issues of T cell, Antigen-presenting cell, Bone marrow and Haplotype in his study of NOD mice. Edward H. Leiter focuses mostly in the field of Insulitis, narrowing it down to matters related to Beta-2 microglobulin and, in some cases, Cellular immunity. His study in Diabetes mellitus is interdisciplinary in nature, drawing from both Gene and Atrophy.
The scientist’s investigation covers issues in Endocrinology, Internal medicine, Immunology, Nod and Diabetes mellitus. His research brings together the fields of Streptozotocin and Internal medicine. The various areas that Edward H. Leiter examines in his Nod study include Congenic, Molecular biology and Bone marrow.
The Congenic study combines topics in areas such as Genetic marker, Haplotype, Inbred strain and Locus. His Diabetes mellitus research includes themes of Phenotype and Obesity. His NOD mice research includes elements of MHC class I, MHC class II and Antigen-presenting cell.
Edward H. Leiter mainly focuses on NOD mice, Genetics, Immunology, Nod and Internal medicine. As part of the same scientific family, Edward H. Leiter usually focuses on NOD mice, concentrating on Insulitis and intersecting with Gene mutation and Leptin receptor. His Adoptive cell transfer, Interleukin 10 and Antigen-presenting cell study in the realm of Immunology connects with subjects such as CD38.
His Nod research is multidisciplinary, incorporating perspectives in Transgene, CD8, Molecular biology, Autoimmunity and Superoxide. His Internal medicine research integrates issues from Diabetes mellitus, Endocrinology and Type 2 diabetes. He works mostly in the field of Congenic, limiting it down to topics relating to Allele and, in certain cases, Major histocompatibility complex.
Edward H. Leiter mostly deals with Molecular biology, Endocrinology, Immunology, Internal medicine and Nod. His studies in Molecular biology integrate themes in fields like Cell growth, Apoptosis, Programmed cell death, Nicotinamide adenine dinucleotide and Signal transduction. Endocrinology and Pharmacogenetics are frequently intertwined in his study.
His study in Interleukin 10, Bone marrow, Autoimmunity, NOD mice and Bacterial antigen is carried out as part of his studies in Immunology. Internal medicine connects with themes related to Diabetes mellitus in his study. His Nod study integrates concerns from other disciplines, such as Glutathione peroxidase, Glutathione reductase, Free-radical theory of aging, Nitrotyrosine and Pancreatic islets.
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The NOD mouse model of type 1 diabetes: as good as it gets?
Mark A. Atkinson;Edward H. Leiter.
Nature Medicine (1999)
B lymphocytes are essential for the initiation of T cell-mediated autoimmune diabetes: analysis of a new "speed congenic" stock of NOD.Ig mu null mice.
D V Serreze;H D Chapman;D S Varnum;M S Hanson.
Journal of Experimental Medicine (1996)
Adoptive Transfer of Diabetes Into Immunodeficient NOD-scid/scid Mice: Relative Contributions of CD4+ and CD8+ T-Cells From Diabetic Versus Prediabetic NOD.NON-Thy-1a Donors
Sherri W Christianson;Leonard D Shultz;Edward H Leiter.
B Lymphocytes Are Critical Antigen-Presenting Cells for the Initiation of T Cell-Mediated Autoimmune Diabetes in Nonobese Diabetic Mice
David V. Serreze;Sara A. Fleming;Harold D. Chapman;Scott D. Richard.
Journal of Immunology (1998)
Therapeutic effects of dehydroepiandrosterone (DHEA) in diabetic mice.
D L Coleman;E H Leiter;R W Schwizer.
Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice.
Michal Prochazka;Edward H. Leiter;David V. Serreze;Douglas L. Coleman.
Major Histocompatibility Complex Class I-Deficient NOD-B2mnull Mice are Diabetes and Insulitis Resistant
David V Serreze;Edward H Leiter;Gregory J Christianson;Dale Greiner.
The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency.
M Prochazka;H R Gaskins;L D Shultz;E H Leiter.
Proceedings of the National Academy of Sciences of the United States of America (1992)
Beta 2-microglobulin-deficient NOD mice do not develop insulitis or diabetes.
Linda S Wicker;Edward H Leiter;John A Todd;Robert J Renjilian.
Lipid metabolome-wide effects of the PPARγ agonist rosiglitazone
Steven M. Watkins;Peter R. Reifsnyder;Huei Ju Pan;J. Bruce German.
Journal of Lipid Research (2002)
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