Protection of IFN-{gamma} signaling-deficient NOD mice from diabetes by cyclophosphamide.

Protection of IFN-{gamma} signaling-deficient NOD mice from diabetes by cyclophosphamide. Research Abstract Details 

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Protection of IFN-{gamma} signaling-deficient NOD mice from diabetes by cyclophosphamide. Abstract Text:

Non-obese diabetic (NOD) mice that are genetically deficient in either IFN-gamma or beta chain of the IFN-gammaR develop diabetes with similar kinetics to wild-type NOD mice. In the current study, we demonstrated that treatment of IFN-gamma signaling-deficient NOD mice with cyclophosphamide (CY) not only fails to induce acute diabetes but also confers permanent protection from diabetes. Protection was mediated by the preferential generation of regulatory T cells (Treg cells) that are capable of suppressing the diabetogenic process, with no change in the total number and function of Treg cells. Moreover, CY treatment of IFN-gamma signaling-deficient NOD mice reversed the ongoing pathogenic process and eliminated cellular infiltrates of pancreatic islets. While these results have been derived using a genetically modified mouse model of diabetes, they indicate that knowledge of host genetic factors and environmental factors influencing the development of Type I diabetes mellitus may provide a rational approach to develop a means to reverse the development of Type I diabetes in human.

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Protection of IFN-{gamma} signaling-deficient NOD mice from diabetes by cyclophosphamide. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: International immunology

VOLUME: 20

Page Numbers: 1231-7

Journal Abbreviation: Int. Immunol.

ISSN: 1460-2377

DAY: 21

MONTH: 07

YEAR: 2008

Protection of IFN-{gamma} signaling-deficient NOD mice from diabetes by cyclophosphamide. Information

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LANGUAGE: eng

NlmUniqueID: 8916182

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AFFILIATION: Laboratory for Autoimmune Regulation.

Country: England

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MEDLINETA: Int Immunol

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