In contrast, long-lived central memory T-cells may persist even after successful treatment of tuberculosis and are less likely to release IFN-c after short incubation with antigen while they are more likely to produce IL-2 upon antigen exposure than effector cells. Thus, assaying M. tuberculosis-specific T cell function defined solely by the quantification of IFN-c secretion after short term ex vivo incubation with M. tuberculosis-specific antigen may prove to be an insufficient indicator for recent inhalation exposure to M. tuberculosis. In contrast, simultaneous measures of other T cell function, such as M. tuberculosis-specific stimulation of IL-2 secretion may improve the discrimination of active versus remote LTBI. These results contrast with studies on other channels and transporters in Xenopus oocytes that reported similar activation effects of SGK and SGKS422D on the Na + coupled glucose transporter SGLT1 and the voltage-gated sodium channel SCN5A. This suggests that SGK activation of ENaC may be controlled differently to SGLT1 and SCN5A, or that the SGK signalling pathway differs between Xenopus oocytes and FRT cells. Finally, our functional data show the importance of the PY motif of SGK in mediating its ability to prevent Nedd4-2 inhibition of ENaC, extending previous reports. IL-17 has been involved in many pathological features that play a role in SSc pathology including the secretion of pro-inflammatory cytokines, the recruitment of monocytes and the triggering of granulocyte-macrophage colony-stimulating factor. In light of fibrosis being the cardinal feature of SSc, it is interesting to note that IL-17 has also been implicated in fibrosis of the basal membrane in asthma and the control of inflammatory response after bleomycin-induce lung injury, a model often exploited to study pulmonary fibrosis. Upon stimulation of cell proliferation, cytoplasmic nucleolin is translocated to the cell surface. Cell surface nucleolin serves as a low affinity receptor for HIV-1 and binds various growth factors via interaction with its GAR domain and lactoferrin). The GAR domain was further demonstrated to be the binding site of HB-19 pseudopeptide which was demonstrated to block nucleolin function as a low affinity receptor on the cell surface. SAR131675 Nevertheless, retinal vascularization was not entirely unaffected after astrocyte VEGF deletion. Speed of angiogenesis, endothelial cell proliferation and survival were all subtly but reproducibly reduced. Every one of these features suggests that there is reduced VEGF activity in the retina during development, which is consistent with our experimental design that targeted only a subpopulation of cells in the retina. Interestingly, deletion of HIF1a had no effect on the development of the retinal vasculature, suggesting that in retinal astrocytes, the primary regulation of VEGF expression is HIF1a-independent.