A Consistent Framework for Coupling Basal Friction With Subglacial Hydrology on Hard-Bedded Glaciers.

Below hard-bedded glaciers, both basal friction and distributed subglacial drainage are thought to be controlled by a network of cavities. Previous coupled hydro-mechanical models, however, describe cavity-driven friction and hydraulic transmissivity independently, resulting in a physically inconsistent cavity evolution between the two components of the models. Here, we overcome this issue by describing the hydro-mechanical system using a common cavity-evolution description, that governs both transient friction and hydraulic transmissivity. We show that our coupling approach is superior to previous formulations in explaining a unique observation record of glacier sliding speed from the French Alps. We find that, at multi-day to multi-decadal timescales, sliding speed can be expressed as a direct function of basal shear stress and water discharge, without accounting for water pressure, which simply adjusts to maintain the cavitation ratio needed to accommodate the water supply.

S100A9 protein is a novel ligand for the CD85j receptor and its interaction is implicated in the control of HIV-1 replication by NK cells.

BACKGROUND: The reportedly broad expression of CD85j across different immune cell types suggests an importance for this molecule in the human immune system. Previous reports have shown that this receptor interacts with several HLA class-I molecules, as well as with some viral proteins. We have demonstrated that the subset of CD85j + Natural Killer (NK) cells efficiently controls human immunodeficiency virus type 1 (HIV-1) replication in monocyte-derived dendritic cells (MDDC) in vitro and this led us to hypothesize that the CD85j + NK cell-mediated anti-HIV activity in MDDC is specifically dependent on the interaction between the CD85j receptor and unknown non-HLA class-I ligand(s). RESULTS: In this study, we focused our efforts on the identification of these non-described ligands for CD85j. We found that the CD85j receptor interacts with a calcium-binding proteins of the S100 family; namely, S100A9. We further demonstrated that HIV-1 infection of MDDC induces a modulation of S100A9 expression on surface of the MDDC, which potentially influences the anti-HIV-1 activity of human NK cells through a mechanism involving CD85j ligation. Additionally, we showed that stimulation of NK cells with exogenous S100A9 enhances the control of HIV-1 infection in CD4+ T cells. CONCLUSIONS: Our data show that S100A9 protein, through ligation with CD85j, can stimulate the anti-HIV-1 activity of NK cells.

Rate-and-state friction explains glacier surge propagation.

The incomplete understanding of glacier dynamics is a major source of uncertainty in assessments of sea-level rise from land-based ice. Through increased ice discharge into the oceans, accelerating glacier flow has the potential to considerably enhance expected sea-level change, well ahead of scenarios considered by the IPCC. Central in our incomplete understanding is the motion at the glacier bed, responsible for flow transients and instabilities involving switches from slow to fast flow. We introduce a rate-and-state framework for the transient evolution of basal shear stress, which we incorporate in glacier simulations. We demonstrate that a velocity-strengthening-weakening transition combined with a characteristic length scale for the opening of subglacial cavities is sufficient to reproduce several previously unexplained features of glacier surges. The rate-and-state framework opens for new ways to analyze, understand and predict transient glacier dynamics as well as to assess the stability of glaciers and ice caps.

Dynamic vulnerability revealed in the collapse of an Arctic tidewater glacier.

Glacier flow instabilities can rapidly increase sea level through enhanced ice discharge. Surge-type glacier accelerations often occur with a decadal to centennial cyclicity suggesting internal mechanisms responsible. Recently, many surging tidewater glaciers around the Arctic Barents Sea region question whether external forces such as climate can trigger dynamic instabilities. Here, we identify a mechanism in which climate change can instigate surges of Arctic tidewater glaciers. Using satellite and seismic remote sensing observations combined with three-dimensional thermo-mechanical modeling of the January 2009 collapse of the Nathorst Glacier System (NGS) in Svalbard, we show that an underlying condition for instability was basal freezing and associated friction increase under the glacier tongue. In contrast, continued basal sliding further upstream increased driving stresses until eventual and sudden till failure under the tongue. The instability propagated rapidly up-glacier, mobilizing the entire 450 km2 glacier basin over a few days as the till entered an unstable friction regime. Enhanced mass loss during and after the collapse (5-7 fold compared to pre-collapse mass losses) combined with regionally rising equilibrium line altitudes strongly limit mass replenishment of the glacier, suggesting irreversible consequences. Climate plays a paradoxical role as cold glacier thinning and retreat promote basal freezing which increases friction at the tongue by stabilizing an efficient basal drainage system. However, with some of the most intense atmospheric warming on Earth occurring in the Arctic, increased melt water can reduce till strength under tidewater glacier tongues to orchestrate a temporal clustering of surges at decadal timescales, such as those observed in Svalbard at the end of the Little Ice Age. Consequently, basal terminus freezing promotes a dynamic vulnerability to climate change that may be present in many Arctic tidewater glaciers.

Natural killer cell responses to dendritic cells infected by the ANRS HIV-1 vaccine candidate, MVAHIV.

Innate mechanisms are critical for the development of the host immune responses to antigen. Particularly, early interaction between natural killer (NK) cells and dendritic cells (DC) greatly impacts the establishment of both innate and adaptive immune responses. In this study, using an autologous in vitro co-culture system we analyzed the NK cell response against MVAHIV-infected DC as well as the subsequent ability of these MVAHIV-primed NK cells to control HIV-1 infection in autologous DC. We found that NK cells responded early to MVAHIV- or MVAWT-infected DC in terms of degranulation and cytokine production. After a 4-day priming of NK cells by MVAHIV- or MVAWT-infected DC we observed an enhanced proliferation and modulation in the NK cell receptor repertoire expression. Interestingly, we found that MVAHIV-primed NK cells had a significant higher ability to control HIV-1 infection in autologous DC compared to MVAWT-primed NK cells; and this enhanced anti-HIV-1 activity appeared to be HIV-specific as MVAHIV-primed NK cells did not have a better ability to control other viral infections or respond against tumoral cells. Furthermore, we observed that NK cell receptors NKG2D and NKp46 modulate the priming of NK cells. This data provides evidence that in vitro NK cells can be primed by viral vector-infected DC, in the context of a NK/DC culture, to specifically target viral infected cells.