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Prostaglandin B(2) delivers a co-stimulatory signal leading to T cell activation.
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2000
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T-regulatory CellImmunologyImmune RegulationTyrosine Kinase ActivitiesImmunologic MechanismImmunotherapyCellular PhysiologyAncillary SignalCo-stimulatory SignalInflammationSignaling PathwayCell SignalingAllergyAutoimmunityProstaglandin BCell BiologyT Cell ActivationCytokineSignal TransductionImmune Cell DevelopmentJurkat CellsCellular Immune ResponseMedicineImmune Cell Activation
Most of the data accumulated to date on the immunoregulatory effects of prostaglandins (PG) on T cell activation stem from the archetypal inhibitory effect of PGE(2). In this study we provide instead, the first evidence that exogenous PGB(2), a catabolic metabolite of PGE(2), synergizes with signals delivered by T cell receptor (TCR) engagement to induce interleukin-2 (IL-2) production and IL-2 receptor (IL-2R) alpha-expression in Jurkat cells. Accordingly, PGB(2) enhances the proliferation of anti-CD3-activated peripheral blood lymphocytes (PBL). In terms of cellular signaling, we present evidence that PGB(2) activates tyrosine kinase activities and efficiently increases c-fos mRNA expression and nuclear factor-kappa B (NF-kappa B) translocation to the nucleus. Owing to these features, PGB(2) appears as a new lipid mediator capable of delivering an ancillary signal leading to T lymphocyte activation.