These multifunctional lectins can hierarchically control a cascade of immunoregulatory events including the expansion, recruitment, and function of regulatory T cells, the promotion of tolerogenic

dendritic cells, and the execution of T-cell death programs. In addition, galectins can control cell adhesion and signaling events critical for implantation and are involved in fundamental processes linking tissue hypoxia to angiogenesis. In an attempt to integrate the regulatory roles of galectins to immunological and vascular programs operating during pregnancy. Here we outline the regulated expression and function of individual members of the galectin family within the fetoplacental unit and their biological implications for the development and preservation of successful pregnancies. “
“The binding of NKG2D to its ligands strengthens learn more the cross-talk between natural killer (NK) cells and dendritic

cells, particularly at early stages, before the initiation of the adaptive immune response. We found that retinoic acid early transcript-1ε (RAE-1ε), one of the ligands of NKG2D, was persistently expressed on antigen-presenting cells in a transgenic mouse model (pCD86-RAE-1ε). By contrast, NKG2D expression on NK cells, NKG2D-dependent cytotoxicity and tumour rejection, and dextran sodium sulphate-induced colitis were all down-regulated in this mouse model. The down-regulation of c-Met inhibitor NKG2D on NK cells was reversed by stimulation with poly (I:C). The ectopic expression of RAE-1ε on dendritic cells maintained NKG2D expression levels and stimulated the activity of NK cells ex vivo, but the higher frequency of CD4+ NKG2D+ T cells in transgenic mice led to the down-regulation of NKG2D on NK cells in vivo. Hence, high levels of RAE-1ε expression on antigen-presenting cells would be expected to induce the down-regulation of NK cell activation by a regulatory T-cell subset.

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“Bystander activation of T cells, i.e. the stimulation of unrelated (heterologous) T cells by cytokines during an Ag-specific T-cell response, has been best described for CD8+ T cells. In the CD8+ compartment, the release of IFN and IFN-inducers leads to the production of IL-15, which mediates the proliferation of CD8+ T cells, notably memory-phenotype CD8+ T cells. CD4+ T cells also undergo bystander activation, however, the signals inducing this TCL Ag-nonspecific stimulation of CD4+ T cells are less well known. A study in this issue of the European Journal of Immunology sheds light on this aspect, suggesting that common γ-chain cytokines including IL-2 might be involved in bystander activation of CD4+ T cells. Bystander activation of T cells was first described by Tough and Sprent, showing that different viruses, virus-mimetics such as poly(I:C) or bacterial products such as LPS induced IFN-α/β secretion, which led to the proliferation and expansion of unrelated (heterologous) polyclonal T cells 1, 2.