IL-17+ CD8+ T cells:differentiation, phenotype and role in inflammatory disease

AbstractThe pro-inflammatory cytokine interleukin-17A (IL-17) has been the subject of research by many groups worldwide. IL-17 expression is often associated with a specific subset of CD4+ T cells (the so-called Th17 cells); however various other immune cell subsets can also synthesise and express IL-17, including CD8+ T cells. Here we review recent data regarding the presence of IL-17+ CD8+ T cells (also known as Tc17 cells) in human inflammatory disease, discuss current knowledge regarding the culture conditions required for the differentiation of these cells in humans and mice, and describe key phenotypic and functional features. Collectively, this information may shed light on the potential pathogenic role that IL-17+ CD8+ T cells may play in human inflammatory disease

Reduced reproductive success in small populations of the self-incompatible Primula vulgaris

Infection of primary CD4+ T cells with HIV-1 coincides with an increase in glycolysis. We investigated the expression of glucose transporters (GLUT) and glycolytic enzymes in human CD4+ T cells in response to infection with HIV-1. We demonstrate the co-expression of GLUT1, GLUT3, GLUT4, and GLUT6 in human CD4+ T cells after activation, and their concerted overexpression in HIV-1 infected cells. The investigation of glycolytic enzymes demonstrated activation-dependent expression of hexokinases HK1 and HK2 in human CD4+ T cells, and a highly significant increase in cellular hexokinase enzyme activity in response to infection with HIV-1. HIV-1 infected CD4+ T cells showed a marked increase in expression of HK1, as well as the functionally related voltage-dependent anion channel (VDAC) protein, but not HK2. The elevation of GLUT, HK1, and VDAC expression in HIV-1 infected cells mirrored replication kinetics and was dependent on virus replication, as evidenced by the use of reverse transcription inhibitors. Finally, we demonstrated that the upregulation of HK1 in HIV-1 infected CD4+ T cells is independent of the viral accessory proteins Vpu, Vif, Nef, and Vpr. Though these data are consistent with HIV-1 dependency on CD4+ T cell glucose metabolism, a cellular response mechanism to infection cannot be ruled out