Central Nervous System Destruction Mediated by Glutamic Acid Decarboxylase-Specific CD4+ T Cells

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Central nervous system destruction mediated by glutamic acid decarboxylase-specific CD4+ T cells.

High titers of autoantibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from type 1 diabetes as well as stiff-person syndrome (SPS), a disorder that affects the CNS, and a variant of SPS, progressive encephalomyelitis with rigidity and myoclonus. Although there is a considerable amount of data focusing on the role of GAD65-specific CD4(+) T cells i...

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Glutamic Acid Decarboxylase-Derived Epitopes with Specific Domains Expand CD4+CD25+ Regulatory T Cells

BACKGROUND CD4(+)CD25(+) regulatory T cell (Treg)-based immunotherapy is considered a promising regimen for controlling the progression of autoimmune diabetes. In this study, we tested the hypothesis that the therapeutic effects of Tregs in response to the antigenic epitope stimulation depend on the structural properties of the epitopes used. METHODOLOGY/PRINCIPAL FINDINGS Splenic lymphocytes...

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Cytotoxic T cells specific for glutamic acid decarboxylase in autoimmune diabetes

Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease that results in the destruction of the pancreatic islet beta cells. Glutamic acid decarboxylase (GAD) has been recently indicated as a key autoantigen in the induction of IDDM in nonobese diabetic mice. In human diabetes, the mechanism by which the beta cells are destroyed is still unknown. Here we report the first evidence for...

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ژورنال

عنوان ژورنال: The Journal of Immunology

سال: 2010

ISSN: 0022-1767,1550-6606

DOI: 10.4049/jimmunol.0903728