BCG Vaccination Prevents Insulin-Dependent Diabetes Mellitus (IDDM) in NOD Mice after Disease Acceleration with Cyclophosphamide

1997 ◽  
Vol 10 (3) ◽  
pp. 271-278 ◽  
Author(s):  
Hui-Yu Qin ◽  
Bhagirath Singh
Keyword(s):  
Diabetes Mellitus ◽  
Nod Mice ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Bcg Vaccination ◽  
Insulin Dependent

scholarly journals Viruses as therapeutic agents. I. Treatment of nonobese insulin-dependent diabetes mice with virus prevents insulin-dependent diabetes mellitus while maintaining general immune competence.

1990 ◽  
Vol 171 (6) ◽  
pp. 2077-2089 ◽  
Author(s):  
M B Oldstone
Keyword(s):  
Diabetes Mellitus ◽  
Autoimmune Diabetes ◽  
Nod Mice ◽  
Insulin Dependent Diabetes Mellitus ◽  
Lymphocytic Infiltration ◽  
Lymphocytic Choriomeningitis ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Beta Cell Destruction ◽  
Insulin Dependent

A situation in which virus can be used as a therapeutic agent to prevent a lethal autoimmune disease is explored. Nonobese insulin-dependent diabetes (NOD) mice spontaneously develop insulin-dependent diabetes mellitus (IDDM), characterized by lymphocytic infiltration into the islets of Langerhans and beta cell destruction, resulting in hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Infection of NOD mice with lymphocytic choriomeningitis virus (LCMV) aborts the autoimmune manifestations and resultant IDDM. The viruses' effect is on a subset of CD4+ lymphocytes. Ablating this autoimmune diabetes does not significantly alter immune responses to a variety of non-LCMV antigens that require CD4+ lymphocyte participation. The prevention of IDDM associated with viral therapy is maintained throughout the life spans of NOD mice.

scholarly journals Immunotherapy for insulin-dependent diabetes mellitus

1995 ◽  
Vol 41 (4) ◽  
pp. 43-48
Author(s):  
I. I. Dedov ◽  
I. A. Abugova ◽  
M. Sh. Shamhalova ◽  
P. I. Shishko
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Interleukin 1 ◽  
Hla Antigens ◽  
Nod Mice ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Tnf Alpha ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent

The autoimmune nature of insulin-dependent diabetes mellitus (IDDM) is currently undeniable. In the 80s, some features of its pathogenesis were determined: on beta cells of patients with newly diagnosed IDDM, overexpression of class I HLA antigens was detected; on beta and alpha cells of isolated islets of Langerhans, expression of class II HLA antigens in combination with tumor necrosis factor (TNF-alpha) and gamma-interferon (gamma-IF) was detected; the presence or absence of Asp-57 in the N-end of the beta1 domain of the HLADQ beta chain has been shown to be positively associated with IDDM in humans and NOD mice; it was revealed that macrophage interleukin-1 (IL-1) and TNF-alpha have a damaging effect on beta cells: IL-1 exhibits selective beta-cell cytotoxicity in low molar concentrations, and the effect of IL-1 is potentiated by TNF-alpha; it was determined that early infiltration during the development of inflammation of pancreas in BB rats is caused by macrophages and monocytes; destruction of beta cells is performed by T-helpers and natural killers. Thus, the autoimmune concept of the disease necessitates the use of immunotherapy to slow the development of IDDM.

Prevention of onset in an insulin-dependent diabetes mellitus model, NOD mice, by oral feeding ofLactobacillus casei

Apmis ◽  
1997 ◽  
Vol 105 (7-12) ◽  
pp. 643-649 ◽  
Author(s):  
TAKESHI MATSUZAKI ◽  
YURIKO NAGATA ◽  
SHOUICHI KADO ◽  
KAZUMI UCHIDA ◽  
IKUO KATO ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Nod Mice ◽  
Insulin Dependent Diabetes Mellitus ◽  
Oral Feeding ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent

scholarly journals Viruses as therapeutic agents. II. Viral reassortants map prevention of insulin-dependent diabetes mellitus to the small RNA of lymphocytic choriomeningitis virus.

1990 ◽  
Vol 171 (6) ◽  
pp. 2091-2100 ◽  
Author(s):  
M B Oldstone ◽  
R Ahmed ◽  
M Salvato
Keyword(s):  
Diabetes Mellitus ◽  
Islets Of Langerhans ◽  
Nod Mice ◽  
Insulin Dependent Diabetes Mellitus ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Pancreatic Islets Of Langerhans ◽  
Insulin Dependent

Nonobese diabetic (NOD) mice are the experimental prototype of type 1 insulin-dependent diabetes mellitus (IDDM). These mice develop a characteristic autoimmune lesion in the pancreatic islets of Langerhans, where infiltrating lymphocytes destroy beta cells, resulting in hypoinsulinemia, hyperglycemia, ketoacidosis, and death. This IDDM, which closely resembles that in humans, is prevented by infecting NOD mice with particular strains of lymphocytic choriomeningitis virus (LCMV), including Armstrong 53b, Traub, WE, and Pasteur. In contrast, the LCMV Armstrong 53b variant, Clone 13, fails to abort IDDM. Hence, although Clone 13 establishes a persistent infection that endures throughout the life spans of NOD mice, their hyperglycemia, hypoinsulinemia, and lymphocytic infiltration into the islets of Langerhans still occur. Genetic reassortant viruses generated between the IDDM therapeutic strain of LCMV Pasteur and the nontherapeutic variant, LCMV Clone 13, were used to treat NOD mice. By using such reassortants and both parental strains of virus to infect NOD mice, the prevention of IDDM was mapped to the S RNA segment of LCMV Pasteur.

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