Related Experiment Video
Updated: Jul 13, 2026

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
Modification of adverse inflammation is required to cure new-onset type 1 diabetic hosts
Maria Koulmanda1, Ejona Budo, Susan Bonner-Weir
1Department of Surgery, Harvard Medical School, and Islet Transplantation Research Laboratory, Massachusetts General Hospital, Boston, MA 02115, USA. mkoulman@bidmc.harvard.edu
Abstract:
In nonobese diabetic (NOD) mice with overt new-onset type 1 diabetes mellitus (T1DM), short-term treatment with a "triple-therapy" regimen [rapamycin plus agonist IL-2-related and antagonist-type, mutant IL-15-related Ig fusion proteins (IL-2.Ig and mutIL-15.Ig)] halts autoimmune destruction of insulin-producing beta cells and restores both euglycemia and immune tolerance to beta cells. Increases in the mass of insulin-producing beta cells or circulating insulin levels were not linked to the restoration of euglycemia. Instead, the restoration of euglycemia was linked to relief from an inflammatory state that impaired the host's response to insulin. Both restoration of immune tolerance to beta cells and relief from the adverse metabolic effects of an inflammatory state in insulin-sensitive tissues appear essential for permanent restoration of normoglycemia in this T1DM model. Thus, this triple-therapy regimen, possessing both tolerance-inducing and select antiinflammatory properties, may represent a prototype for therapies able to restore euglycemia and self-tolerance in T1DM.
Related Concept Videos
Type I Diabetes II: Pathophysiology
Type I Diabetes I: Introduction
Diabetes Mellitus: Overview and Type I Subtype
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
Type II Diabetes II: Pathophysiology
Type I Diabetes III: Clinical Manifestations
Diabetes Mellitus: Type 2 and Gestational
