Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBD
Development of autoimmune insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice is an example of a complex multifactorial disease with strong genetic and environmental components. As such, this model may provide insight not only into mouse models of inflammatory bowel disease, but also...
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| Language: | English |
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Wiley
1995-01-01
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| Series: | Canadian Journal of Gastroenterology |
| Online Access: | http://dx.doi.org/10.1155/1995/250285 |
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| author | Edward H Leiter |
| author_facet | Edward H Leiter |
| author_sort | Edward H Leiter |
| collection | DOAJ |
| description | Development of autoimmune insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice is an example of a complex multifactorial disease with strong genetic and environmental components. As such, this model may provide insight not only into mouse models of inflammatory bowel disease, but also may provide insight into how the environment may interact with the genome to initiate pathogenesis in humans. NOD mice are characterized by accumulation of unusually high percentages of T lymphocytes in lymphoid organs. Pancreatic beta cell destruction in NOD mice is T lymphocyte-mediated. Complex interactions between the inherently diabetogenic major histocompatibility complex (MHC) haplotype of this strain and non-MHC-associated insulin-dependent diabetes susceptibility genes (Idd) are required for cytopathic activation of the leukocytic infiltrates in the pancreas (insulitis). Penetrance of the diabetogenic Idd genes is strongly influenced by both dietary and microbiological factors in the environment. Genetic susceptibility is transmitted by hemopoietic stem cells, and specific defects in T immunoregulation have been traced to defects in the development and function of marrow-derived antigen presenting cells. The spontaneous development of diabetes in NOD mice is different from experimentally induced forms of diabetes in mice in several important respects. In addition to the pathognomic development of pancreatic insulitis, the generalized loss of immunoregulatory control of autoreactive T lymphocytes in NOD mice is reflected by development of leukocytic infiltrates into a plethora of organ systems including the submandibular salivary glands, thyroid glands, kidneys and, occasionally, the colon. |
| format | Article |
| id | doaj-art-4bf7cc6255a543bdb0701c7e2bb8b192 |
| institution | Kabale University |
| issn | 0835-7900 |
| language | English |
| publishDate | 1995-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Canadian Journal of Gastroenterology |
| spelling | doaj-art-4bf7cc6255a543bdb0701c7e2bb8b1922025-08-20T03:36:31ZengWileyCanadian Journal of Gastroenterology0835-79001995-01-019315315910.1155/1995/250285Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBDEdward H Leiter0The Jackson Laboratory, Bar Harbor, Maine, USADevelopment of autoimmune insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice is an example of a complex multifactorial disease with strong genetic and environmental components. As such, this model may provide insight not only into mouse models of inflammatory bowel disease, but also may provide insight into how the environment may interact with the genome to initiate pathogenesis in humans. NOD mice are characterized by accumulation of unusually high percentages of T lymphocytes in lymphoid organs. Pancreatic beta cell destruction in NOD mice is T lymphocyte-mediated. Complex interactions between the inherently diabetogenic major histocompatibility complex (MHC) haplotype of this strain and non-MHC-associated insulin-dependent diabetes susceptibility genes (Idd) are required for cytopathic activation of the leukocytic infiltrates in the pancreas (insulitis). Penetrance of the diabetogenic Idd genes is strongly influenced by both dietary and microbiological factors in the environment. Genetic susceptibility is transmitted by hemopoietic stem cells, and specific defects in T immunoregulation have been traced to defects in the development and function of marrow-derived antigen presenting cells. The spontaneous development of diabetes in NOD mice is different from experimentally induced forms of diabetes in mice in several important respects. In addition to the pathognomic development of pancreatic insulitis, the generalized loss of immunoregulatory control of autoreactive T lymphocytes in NOD mice is reflected by development of leukocytic infiltrates into a plethora of organ systems including the submandibular salivary glands, thyroid glands, kidneys and, occasionally, the colon.http://dx.doi.org/10.1155/1995/250285 |
| spellingShingle | Edward H Leiter Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBD Canadian Journal of Gastroenterology |
| title | Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBD |
| title_full | Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBD |
| title_fullStr | Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBD |
| title_full_unstemmed | Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBD |
| title_short | Multifactorial Control of Autoimmune Insulin-Dependent Diabetes in NOD Mice: Lessons for IBD |
| title_sort | multifactorial control of autoimmune insulin dependent diabetes in nod mice lessons for ibd |
| url | http://dx.doi.org/10.1155/1995/250285 |
| work_keys_str_mv | AT edwardhleiter multifactorialcontrolofautoimmuneinsulindependentdiabetesinnodmicelessonsforibd |