Killer immunoglobulin-like receptor expression on single cells: a cautionary note

Natural killer (NK) cells keep the surface expression of major histocompatibility complex (MHC) class I molecules under surveillance using killer immunoglobulin-like receptors (KIR). Virus-infected or aberrant cells are frequently characterized by a reduced surface expression of MHC class I antigens and may therefore be removed by cytolysis. NK cells are heterogeneous with regard to the expression of KIR genes. The resulting subpopulations show distinguishable specificities allowing the recognition of cells lacking varying combinations of MHC class I antigens. The KIR expression pattern in single NK cells has previously been analyzed by Husain and colleagues by cDNA preamplification of CD3(−) CD56(+) single cells and subsequent gene-specific polymerase chain reaction. We show here that the data of this study contain inconsistencies. These inconsistencies are discussed in the context of KIR mRNA abundance and single-cell cDNA amplification efficiency

Ischemic preconditioning acts upstream of GluR2 down-regulation to afford neuroprotection in the hippocampal CA1

Animals subjected to sublethal transient global ischemia (ischemic preconditioning) exhibit neuroprotection against subsequent global ischemia-induced neuronal death in the hippocampal CA1 (ischemic tolerance). The molecular mechanisms underlying ischemic tolerance are unclear. Here we report that ischemic preconditioning induced a small, transient down-regulation of GluR2 mRNA expression and greatly attenuated subsequent ischemia-induced GluR2 mRNA and protein down-regulation and neuronal death. Ischemic preconditioning and GluR2 antisense knockdown acted synergistically to increase cell death. Sublethal antisense knockdown did not protect against subsequent ischemic insults or antisense knockdown. These findings indicate that ischemic preconditioning acts at step(s) upstream from suppression of GluR2 gene expression to afford neuroprotection and implicate transcriptional regulation of GluR2 expression in the adaptive mechanisms associated with ischemic tolerance