Caspase-1 Is Not Required for Type 1 Diabetes in the NOD Mouse

Caspase-1 is not required for type 1 diabetes in the NOD mouse.

Interleukin (IL)-1 beta and IL-18 are two cytokines associated with the immunopathogenesis of diabetes in NOD mice. Both of these cytokines are cleaved by caspase-1 to their biologically active forms. IL-1 is a proinflammatory cytokine linked to beta-cell damage, and IL-18 stimulates production of interferon (IFN)gamma in synergy with IL-12. To examine the effects produced by caspase-1 deficien...

Interleukin-21 Is Required for the Development of Type 1 Diabetes in NOD Mice

OBJECTIVE Interleukin (IL)-21 is a type 1 cytokine that has been implicated in the pathogenesis of type 1 diabetes via the unique biology of the nonobese diabetic (NOD) mouse strain. The aim of this study was to investigate a causal role for IL-21 in type 1 diabetes. RESEARCH DESIGN AND METHODS We generated IL-21R-deficient NOD mice and C57Bl/6 mice expressing IL-21 in pancreatic beta-cells, ...

Reduction of CD4 in the NOD Mouse Is Associated with a Cyclophosphamide-Induced Type-1 Diabetes

Analysis of the Mouse CD 30 Gene A Candidate for the NOD Mouse Type 1 Diabetes

Members of the tumor necrosis factor receptor superfamily play an important role in the initiation, expansion, and termination of an immune response. It has recently been demonstrated that one member of this family, CD30, plays a central role in maintaining peripheral tolerance by controlling the expansion of autoreactive CD8 T-cells. In the present study, Cd30 was mapped to a 5.6-cM interval o...

t-helper cell type-1 transcription factor t-bet is down-regulated in type 1 diabetes

t cells have been identified as key players in the pathogenesis of type 1 diabetes. however, the exact role of t-cell subpopulations in this pathway is presently unknown. the purpose of this study was to assess the expression pattern of two lineage-specifying transcription factors gata - 3 and t - bet , which are important in t helper type 1 (th1) and th2 cell development , respectively. gene e...