Questions to be asked are for example: Is our parameterization of a continuum in ligand degradation rates reasonable or would it be better to model several ligand classes with different degradation rates (Hansell et al., 2012), but also possibly different photoreactivities and stability constants (Barbeau et al., 2003)? Would it be better to make the direct production of ligands near the surface directly dependent on iron limitation of phytoplankton and/or bacteria? Are external sources of ligands, e.g. from rivers (Mikkelsen et al., 2006 and Rijkenberg et al., 2006) important

for the open ocean? Despite this complexity, a general paradigm for ligand cycling has emerged (Hunter and Boyd, 2007 and Gledhill and Buck, 2012) that ABT-888 clinical trial contradicts how ligands are currently simulated in OGCBMs. We have attempted to appraise how such a view can be represented in two OGCBMs and evaluate the controlling mechanisms and impact on Olaparib mw iron cycling. We thank Ying Ye, who started the compilation of ligand data and initiated the prognostic ligand modeling. We also thank the reviewers for their helpful and constructive comments and the Scientific Committee on Oceanic Research (SCOR) by the International Council for Science for travel support. The work of C.V. was supported by the BMBF project SOPRAN under grant agreement 03F0662C. This work made use of the facilities of N8 HPC provided and funded by the N8 consortium

and EPSRC (grant EP/K000225/1) and coordinated by the Universities of Leeds and Manchester. “
“Current Resveratrol Opinion in Immunology 2015, 32:xx–yy This review comes from a themed issue on Innate immunity Edited by Zhijian J Chen and Sebastian Amigorena http://dx.doi.org/10.1016/j.coi.2014.11.001 0952-7915/© 2014 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/3.0/).

DCs were originally identified by Steinman and Cohn in mouse spleen on the basis of their unique morphology, which distinguished them from macrophages [1]. They were subsequently found to be the most potent stimulators of the mixed lymphocyte reaction [2], setting the foundation for decades of research demonstrating the importance of DCs in initiating adaptive immune responses. The name dendritic cell has become synonymous with motile cells of stellate morphology, expressing high levels of major histocompatibility complex class II molecules and the integrin CD11c [3 and 4], distinguished by their ability to migrate from non-lymphoid to lymphoid organs and their superior capacity to stimulate T lymphocytes [5, 6 and 7]. This has been subsumed into the notion that DCs can be defined by their ability to migrate to secondary lymphoid tissues and prime T cells. This definition is useful but excludes the possibility that, in some instances, T cell priming may be carried out by monocytes or macrophages.