A Factor of Inducing IgE from a Filarial Parasite Prevents Insulin-Dependent Diabetes Mellitus in Nonobese Diabetic Mice

2001 ◽  
Vol 286 (5) ◽  
pp. 1051-1058 ◽  
Author(s):  
Shinjiro Imai ◽  
Hiroyuki Tezuka ◽  
Koichiro Fujita
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Dependent Diabetes Mellitus ◽  
Filarial Parasite ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Mice ◽  
Nonobese Diabetic ◽  
Insulin Dependent ◽  
Nonobese Diabetic Mice

scholarly journals Reversal of Spontaneous Autoimmune Insulitis in Nonobese Diabetic Mice by Soluble Lymphotoxin Receptor

2001 ◽  
Vol 193 (11) ◽  
pp. 1327-1332 ◽  
Author(s):  
Qiang Wu ◽  
Benoît Salomon ◽  
Min Chen ◽  
Yang Wang ◽  
Lisa M. Hoffman ◽  
...  
Keyword(s):  
Autoimmune Diabetes ◽  
Critical Role ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Transfer Model ◽  
Diabetic Mice ◽  
Nonobese Diabetic ◽  
Insulin Dependent ◽  
Nonobese Diabetic Mice

One striking feature of spontaneous autoimmune diabetes is the prototypic formation of lymphoid follicular structures within the pancreas. Lymphotoxin (LT) has been shown to play an important role in the formation of lymphoid follicles in the spleen. To explore the potential role of LT-mediated microenvironment in the pathogenesis of insulin-dependent diabetes mellitus (IDDM), an LTβ receptor–immunoglobulin fusion protein (LTβR–Ig) was administered to nonobese diabetic mice. Early treatment with LTβR–Ig prevented insulitis and IDDM, suggesting that LT plays a critical role in the insulitis development. LTβR–Ig treatment at a late stage of the disease also dramatically reversed insulitis and prevented diabetes. Moreover, LTβR–Ig treatment prevented the development of IDDM by diabetogenic T cells in an adoptive transfer model. Thus, LTβR–Ig can disassemble the well established lymphoid microenvironment in the islets, which is required for the development and progression of IDDM.

The development of insulin-dependent diabetes mellitus in non-obese diabetic mice: the role of CD4+ and CD8+ T cells

1991 ◽  
Vol 19 (1) ◽  
pp. 187-191 ◽  
Author(s):  
Anne-Marie Varey ◽  
Patricia Hutchings ◽  
Lorraine O'Reilly ◽  
Tracey Hussell ◽  
Herman Waldmann ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
T Cells ◽  
Cd8 T Cells ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Mice ◽  
Insulin Dependent

scholarly journals Prevention of insulin-dependent diabetes mellitus in nonobese diabetic mice by immunogenic but not by tolerated peptides.

1995 ◽  
Vol 182 (3) ◽  
pp. 897-902 ◽  
Author(s):  
M Vaysburd ◽  
C Lock ◽  
H McDevitt
Keyword(s):  
Diabetes Mellitus ◽  
T Cell Activation ◽  
Insulin Dependent Diabetes Mellitus ◽  
Nod Mouse ◽  
Insulin Dependent Diabetes ◽  
Autoimmune Response ◽  
Dependent Diabetes Mellitus ◽  
Immunogenic Peptide ◽  
Nonobese Diabetic ◽  
Insulin Dependent

In the nonobese diabetic (NOD) mouse, susceptibility to insulin-dependent diabetes mellitus is in part controlled by a single expressed class II major histocompatibility complex (MHC) molecule, I-Ag7. This molecule probably exerts its control through the representation of a self-peptide, derived from an unknown beta cell antigen, leading to T cell activation and eventual islet destruction. In this paper, synthetic peptides have been used to compete for binding to the I-Ag7 molecule in an attempt to suppress the autoimmune response. The administration of an I-Ag7-binding immunogenic peptide, lambda repressor (cI) 12-26, in a water and oil emulsion (incomplete Freund's adjuvant) can prevent the transfer of IDDM into irradiated recipients by spleen cells from diabetic donors. Nonbinding, nonimmunogenic peptides have no effect in this situation. However, the immune response to the "blocking" peptide in these experiments was a complicating factor in interpreting the results. To establish that the effect was at the level of competition for MHC binding, two additional approaches were tried. First, tolerance was induced to the immunogenic peptide, cI 12-26, before using it to "block" disease. Tolerance abolished the effect on diabetes transfer. Second, an effort was made to identify peptides that were nonimmunogenic but that bound to I-Ag7. Such a peptide, mouse prostatic secretory glycoprotein precursor 63-76, had no effect on the incidence of transferred disease. We conclude that the "blocking" effects seen in initial experiments in the NOD mouse were not caused by blockade of MHC presentation, but by other unknown effects related to the immunogenicity of the "blocking" peptide.

Prevention of insulin-dependent diabetes mellitus in non-obese diabetic mice by transgenes encoding modified I-A β-chain or normal I-E α-chain

Nature ◽  
1990 ◽  
Vol 345 (6277) ◽  
pp. 727-729 ◽  
Author(s):  
Torben Lund ◽  
Lorraine O'Reilly ◽  
Patricia Hutchings ◽  
Osami Kanagawa ◽  
Elizabeth Simpson ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Mice ◽  
Insulin Dependent ◽  
Α Chain ◽  
Β Chain
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