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+ populations were sorted from the LN and spleen of male mice. Post sort analysis of GFP vs. YFP (top row) and CD4 vs Foxp3 intracellular staining. (B) Schematic of the Foxp3 locus showing the TSDR amplified for CpG methylation analysis. The TATA box of the promoter is indicated, and Amp represents the region analyzed by bisulphite treatment, amplification(More)
The inducible isoform of the enzyme cyclooxygenase-2 (COX2) is an immediate early gene induced by synaptic activity in the brain. COX2 activity is an important mediator of inflammation, but it is not known whether COX2 activity is pathogenic in brain. To study the role of COX2 activity in ischemic injury in brain, expression of COX2 mRNA and protein and the(More)
In diabetic patients and susceptible mice, insulin is a targeted autoantigen. Insulin B chain 9-23 (B:9-23) autoreactive CD4 T cells are key for initiating autoimmune diabetes in NOD mice; however, little is known regarding their origin and function. To this end, B:9-23-specific, BDC12-4.1 T-cell receptor (TCR) transgenic (Tg) mice were studied, of which,(More)
A fundamental question about the pathogenesis of spontaneous autoimmune diabetes is whether there are primary autoantigens. For type 1 diabetes it is clear that multiple islet molecules are the target of autoimmunity in man and animal models. It is not clear whether any of the target molecules are essential for the destruction of islet beta cells. Here we(More)
The observation that delayed death of CA1 neurons after global ischemia is inhibited by protein synthesis inhibitors suggests that the delayed death of these neurons is an active process that requires new gene expression. Delayed death in CA1 has some of the characteristics of apoptotic death; however, candidate proapoptotic proteins have not been(More)
There is accumulating evidence that autoimmunity to insulin B chain peptide, amino acids 9-23 (insulin B:9-23), is central to development of autoimmune diabetes of the NOD mouse model. We hypothesized that enhanced susceptibility to autoimmune diabetes is the result of targeting of insulin by a T-cell receptor (TCR) sequence commonly encoded in the(More)
T he age of onset of type 1A diabetes is now im-munologically predictable (1). Either because of a lack of sufficient understanding of the patho-genesis of type 1A (immune-mediated) diabetes or a lack of effective therapeutics directed at relevant pathogenic pathways (or both), we cannot yet prevent this disease (2). The article by Liu et al. (3) in this(More)
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