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L'infection à cytomégalovirus (CMV) représente la complication infectieuse la plus fréquente en transplantation d'organes solides pour laquelle le risque est à l'heure actuelle essentiellement stratifié en fonction du statut sérologique anti-CMV du receveur (R) et du donneur (D) avant greffe. Le traitement antiviral se décline selon deux options stratégiques guidées par le statut D/R, la prophylaxie universelle ou la thérapie préemptive. L'immunité cellulaire médiée par les lymphocytes T CD8 et CD4 constituant le mécanisme majeur de la réponse immune anti- CMV, différents tests IGRAs (IFN-γ Release Assays) ont été développés : le test Elisa, QuantiFERON®-CMV et les tests ELIspot :T-Spot® CMV et T-Track® CMV. Ces analyses sont basées sur la mesure de la sécrétion d'IFN-γ par les lymphocytes T effecteurs mémoire spécifiques après leur stimulation par les peptides CMV Cette revue de la littérature présente l'intérêt des tests IGRAs, en complément des données du statut sérologique, pour une meilleure stratification des patients à risque de développer une infection sévère à CMV Elle aborde également la valeur ajoutée du suivi cinétique du contrôle de la réplication virale par les effecteurs T pour l'optimisation de la prise en charge thérapeutique antivirale au cours de la surveillance post-transplantation en complément des données virologiques. Cytomegalovirus (CMV) infection represents the most frequent infectious complication in solid organ transplantation for which the risk is mainly stratified according to the anti-CMV serological status of the recipient (R) and the donor (D) before transplantation. There are two strategic options for antiviral treatment, universal prophylaxis or preemptive therapy. As T-cell response mediated by CD8 and CD4 lymphocytes is the major mechanism of the anti-CMV immune response, multiple IGRAs tests (IFN-γ Release Assays) have been developed: the Elisa test, QuantiFERON®-CMV and the ELIspot tests: T-Spot® CMV and T-Track® CMV These assays are based on the measurement of IFN-γ secretion by specific memory T cells after their stimulation by CMV peptides. This review presents the usefulness of IGRAs tests, in addition to the anti-CMV serological status data, for a better stratification of patients at risk before transplantation. It also discusses the benefit of monitoring of viral replication control by T effectors in order to optimize antiviral therapeutic management during post-transplant monitoring in addition to virological data. [ABSTRACT FROM AUTHOR]

ڐ • An unidentified factor drives platelet production in TPO/Mpl-deficient mice. • EPO is an in vivo residual thrombopoietic factor in the absence of the TPO/Mpl pathway. • EPO and TPO conjointly regulate platelet size, both in physiology and under stress conditions. • EPO might have potential therapeutic use in congenital thrombocytopenia. • EPO stimulation might increase the cardiovascular risk. Thrombopoietin (TPO), through activation of its cognate receptor Mpl, is the major regulator of platelet production. However, residual platelets observed in TPO- and Mpl-loss-of-function (LOF) mice suggest the existence of an additional factor to TPO in platelet production. As erythropoietin (EPO) exhibited both in vitro megakaryocytic potential, in association with other early-acting cytokines, and in vivo platelet activation activity, we sought to investigate its role in this setting. Here, we used multiple LOF models to decipher the reciprocal role of EPO and TPO in the regulation of platelet production in TPO-LOF and Mpl-LOF mice and of platelet size heterogeneity in wild-type mice. We first identified EPO as the major thrombopoietic factor in the absence of the TPO–Mpl pathway. Based on the study of several mouse models we found that the EPO–EPO receptor pathway acts on late-stage megakaryopoiesis and is responsible for large-sized platelet production, while the TPO–Mpl pathway promotes small-sized platelet production. On the basis of our data, EPO might be used for thrombocytopenia supportive therapy in congenital amegakaryocytopoiesis. Furthermore, as a distribution skewed toward large platelets is an independent risk factor and a poor prognosis indicator in atherothrombosis, the characterization of EPO's role in the production of large-sized platelets, if confirmed in humans, may open new perspectives in the understanding of the role of EPO-induced platelets in atherothrombosis. [ABSTRACT FROM AUTHOR]