130,799 research outputs found

    IFN-gamma: a Janus-faced cytokine in dendritic cell programming

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    Discussion on dose-dependent bivalent effects of IFN- in association with the acquisition of regulatory features by DCs

    Are human Vδ2pos T cells really resistant to aging and Human Cytomegalovirus infection?

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    In their recent paper, Weili Xu et al. [1] described the different behaviors of Vδ1pos and Vδ2pos T cell subsets in response to lifelong stress and claimed that Vδ2pos T cells are not affected by aging and Human Cytomegalovirus (HCMV) infection. While we agree that these two γδ T cell subsets diverge both in phenotype/function and in tissue distribution, we are somewhat surprised that authors did not take into account the several previously published and contradictory experimental evidence in regards to senescence of Vδ2pos T cells [2,3]. These latter studies reported that HCMV infection not only induces a clonal expansion of a distinct Vγ9neg/Vδ2pos T cell subset, but also determines a concomitant adaptive differentiation from CD27high naïve cells to CD27low/neg terminal-effectors. However, Weili Xu et al. argued that the expression and kinetics of both CD27 and CD45RA surface markers do not change and follow the homeostatic changes of Vδ2pos T cells. This statement goes in the opposite direction to previously reported findings as the CD27/CD45RA phenotype has been shown to mark the maturation and differentiation (TNaïve, TCentral-Memory, Teffector-Memory and TEffectory-Memory RA) of Vδ2pos T cells. Indeed, the different surface expression of both CD27 and CD45 parallel the progressive decrease of telomere length, the proliferative capacity as well as the different effector-functions and resistance to death of Vδ2+ T cells in response to antigens and homeostatic cytokines [4,5]. Hence, we believe that these controversial issues require further discussion beyond the unilateral conclusion given by the study of Weili Xu et al

    Detection of circulating endothelial progenitor cells in cardiovascular diseases

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    Introduction: Endothelial progenitor cells (EPCs) are bone marrow-derived cells playing a critical role in adult vasculogenesis and endothelial homeostasis, as they are recruited to sites of endothelial injury where they contribute to blood vessel formation and repair. Since their first description in 1997, EPCs have stimulated considerable interest among scientists due to the observation that variations in their number and function are associated with many pathological conditions including cardiovascular, cancer, and metabolic diseases. However, comparative interpretation of clinical studies on EPCs is still hampered by the lack of standardized methods employed for EPC quantification and analysis. Methods: Two main approaches are currently used to study circulating EPCs. One approach consists in identifying and selecting EPCs by cell surface phenotype using fluorescently labeled antibodies and flow cytometry directly performed on peripheral blood samples. The second approach consists in isolating and expanding EPCs in vitro, starting from peripheral blood samples. Key advantages, limits and critical methodological aspects of each approach will be illustrated. Results: EPC variations observed in pathological conditions will be shown, mainly focused on the involvement of EPCs in cardiovascular diseases. The behaviour of EPCs during particular physiologic challenges, such as systemic hypoxia exposure and physical exercise, will also be described in order to provide some insight into the role and function of EPCs in human physiopathology. Conclusions: Changes in the number and function of circulating EPCs may be relevant to the study of a wide range of human diseases. If the methods for studying EPCs will be adequately standardized and adapted for routine use, EPC analysis will likely become a valuable diagnostic and prognostic non-invasive tool useful for patient follow-up
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