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Müller glial cells (MGCs) are known to participate actively in retinal development and to contribute to homoeostasis through many intracellular mechanisms. As there are no homologous cells in other neuronal tissues, it is certain that retinal health depends on MGCs. These macroglial cells are located at the centre of the columnar subunit and have a great ability to interact with neurons, astrocytes, microglia and endothelial cells in order to modulate different events. Several investigations have focused their attention on the role of MGCs in diabetic retinopathy, a progressive pathology where several insults coexist. As expected, data suggest that MGCs display different responses according to the severity of the stimulus, and therefore trigger distinct events throughout the course of the disease. Here, we describe physiological functions of MGCs and their participation in inflammation, gliosis, synthesis and secretion of trophic and antioxidant factors in the diabetic retina. We invite the reader to consider the protective/deleterious role of MGCs in the early and late stages of the disease. In the light of the results, we open up the discussion around and ask the question: Is it possible that the modulation of a single cell type could improve or even re-establish retinal function after an injury?

Because of their plasticity and central role in orchestrating immunity and tolerance, DCs can respond to pregnancy-specific signals, thus promoting the appropriate immune response in order to support pregnancy. Here, we show that pregnancy-specific glycoprotein (PSG1a), the major variant of PSG released into the circulation during pregnancy, targets DCs to differentiate into a subset with a unique phenotype and function. This semimature phenotype is able to secrete IL-6 and TGF-β. PSG1a also affected the maturation of DCs, preventing the up-regulation of some costimulatory molecules, and inducing the secretion of TGF-β or IL-10 and the expression of programmed death ligand 1 (PD-L1) in response to TLR-9 or CD40 ligation. In addition, PSG1a-treated DCs promoted the enrichment of Th2-type cytokines, IL-17-producing cells, and Treg cells from CD4 + T cells from DO11.10 Tg mice. Moreover, in vivo expression of PSG1a promoted the expansion of Ag-specific CD4 + CD25 + Foxp3 + Treg cells and IL-17-, IL-4-, IL-5-, and IL-10-secreting cells able to protect against Listeria monocytogenes infection. Taken together, our data indicate that DCs can be targeted by PSG1a to generate the signals necessary to mount an appropriate, well-balanced, and effective immune response able to protect against invading pathogens while at the same time being compatible with a successful pregnancy. Keywords: Pregnancy IntroductionDCs are a heterogeneous population of highly specialized APCs recognized for their crucial role as regulators of innate and adaptive immunity. They can also fine tune the context (and hence the outcome) of Ag presentation in response to a plethora of environCorrespondence: Prof. Claudia C. Motrán e-mail: cmotran@fcq.unc.edu.ar mental signals that indicate the presence of pathogens or tissue damage. These signals generally boost DC maturation, which promotes their migration from peripheral tissues to secondary lymphoid organs and increases their capacity to induce and regulate effector T-cell responses. In addition, recent evidence has highlighted a critical role for DCs in promoting tolerance, limiting uncontrolled inflammation and maintaining immune cell homeostasis [1].The DC-derived factors that determine the outcome of DC-T-cell interactions are the levels of Ag presentation, the display of costimulatory molecules, and the presence ofwww.eji-journal.eu 1574 Fernando F. Martínez et al. Eur. J. Immunol. 2012. 42: 1573-1584 immunomodulatory factors such as cytokines. While increased levels of Ag presentation and the expression of costimulatory molecules such as CD80, CD86, and CD40 on DCs are crucial for the expansion of Ag-specific T cells, the expression of coinhibitory molecules, such as programmed cell death-1 (PD-1) ligands, PD-L1 and PD-L2, can act synergistically to inhibit T-cell activation, proliferation, and cytokine production [2]. Regarding the role of cytokine in driving the type of cellular effector response, stimuli that induce IL-12 promote IFN-γ-producing Th1 cells, stimuli that induce IL-10 and T...