Prevention of diabetes mellitus in the non-obese diabetic mouse strain with monoclonal antibodies against the CD45RB molecule
MM Abu-Hadid, AI Lazarovits, J Madrenas - Autoimmunity, 2000 - Taylor & Francis
MM Abu-Hadid, AI Lazarovits, J Madrenas
Autoimmunity, 2000•Taylor & FrancisInsulin dependent diabetes mellitus (IDDM) is an organ specific T-cell mediated
autoimmune disease characterized by hyperglycemia secondary to specific destruction of P-
cells in the pancreas."'21 The non-obese diabetic (NOD) mouse strain develops
spontaneous diabetes mellitus following interactions between genetic and environmental
factors, and serves as a model for human IDDM.[3'I In this mouse strain, progression towards
autoimmune diabetes occurs in three distinct but overlapping stages.[*'The first stage is …
autoimmune disease characterized by hyperglycemia secondary to specific destruction of P-
cells in the pancreas."'21 The non-obese diabetic (NOD) mouse strain develops
spontaneous diabetes mellitus following interactions between genetic and environmental
factors, and serves as a model for human IDDM.[3'I In this mouse strain, progression towards
autoimmune diabetes occurs in three distinct but overlapping stages.[*'The first stage is …
Insulin dependent diabetes mellitus (IDDM) is an organ specific T-cell mediated autoimmune disease characterized by hyperglycemia secondary to specific destruction of P-cells in the pancreas."'21 The non-obese diabetic (NOD) mouse strain develops spontaneous diabetes mellitus following interactions between genetic and environmental factors, and serves as a model for human IDDM.[3'I In this mouse strain, progression towards autoimmune diabetes occurs in three distinct but overlapping stages.[*'The first stage is characterized by mononuclear infiltration (with high representation of T cells) of the pancreatic islets of Langerhan. This stage starts at approximately three weeks of age and occurs both in male and female NOD mice. The second stage, also shared by male and female NOD mice, is characterized by the development of insulitis. Almost immediately upon arrival, the mononuclear cells start invading the pancreatic islets causing inflammation in the islets of Langerhan (benign ins~ litis).~~~ The final stage is the destruction of insulin producing p-cells in the pancreatic islets of Langerhan (malignant insuliti~).'~] Destruction of 90% or more of these cells correlates with hypoinsulinemia and subsequently hyperglycemia. In NOD mice this
