Ontology highlight
ABSTRACT: Background
Non-obese diabetic (NOD) mice exhibit autoimmune diabetes and Sjögren's-like syndrome.Objective
To test whether a treatment that reverses end-stage diabetes in the NOD mouse would affect their Sjögren's-like syndrome.Methods
NOD mice have a proteasome defect. Improperly selected naive T cells escape, but can be killed by reintroducing major histocompatibility complex class I self-peptides on matched normal splenocytes. The proteasome defect also impairs nuclear factor kB, a transcription factor in pathogenic memory T cells, increasing their susceptibility to tumour necrosis factor-induced apoptosis stimulated through complete Freund's adjuvant (CFA). The impact of this two-limb therapy (injections of matched normal splenocytes and CFA) on the autoimmune s
SUBMITTER: Tran SD
PROVIDER: S-EPMC1954678 | biostudies-literature | 2007 Jun
REPOSITORIES: biostudies-literature