Spread between the euro short-term rate (€STR) and the deposit facility rate

Rationale This article analyses the factors that are contributing to the widening of the spread between the euro short-term rate (€STR) and the deposit facility rate, with a view to assessing monetary policy transmission in the Eurosystem. Takeaways •The key factors that explain the behaviour of this spread are the expansion of the Eurosystem’s balance sheet and the change in the monetary policy stance. •The pass-through of the recent interest rate hikes to money market rates has been effective and cannot explain the widening of the spread. •Once the rate hiking cycle comes to an end, the contraction in the Eurosystem’s balance sheet can be expected to curb or even reverse the trend observed in the spread

Diferencial entre el €STR y el tipo de interés de la facilidad de depósito

Motivación Este artículo analiza los factores que estarían contribuyendo al incremento del diferencial existente entre el Euro short-term rate y el tipo de interés de la facilidad de depósito, con el objetivo de valorar la transmisión de la política monetaria en el Eurosistema. Ideas principales •Los principales factores que explican la evolución del diferencial son el aumento en el balance del Eurosistema y el cambio en la orientación de la política monetaria. •La transmisión de las recientes subidas de tipos de interés oficiales a los tipos de interés del mercado monetario fue efectiva, por lo que no es un factor explicativo del incremento del diferencial. •Cabría esperar que, una vez concluido el ciclo alcista de tipos, la reducción del balance del Eurosistema frenase o incluso revirtiese la tendencia observada en el diferencial

Enhanced susceptibility of galectin-1 deficient mice to experimental colitis

Este trabajo fue subvencionado por el Instituto de Salud Carlos III y cofinanciado por el Fondo Europeo de Desarrollo Regional (FEDER)Galectin-1 is aβ-galactoside-binding lectin, ubiquitously expressed in stromal, epithelial, and different subsets of immune cells. Galectin-1 is the prototype member of the galectin family which shares specificity withβ-galactoside containing proteins and lipids. Immunomodulatory functions have been ascribed to endogenous galectin-1 due to its induction of T cell apoptosis, inhibitory effects of neutrophils and T cell trafficking. Several studies have demonstrated that administration of recombinant galectin-1 suppressed experimental colitis by modulating adaptive immune responses altering the fate and phenotype of T cells. However, the role of endogenous galectin-1 in intestinal inflammation is poorly defined. In the present study, the well-characterized acute dextran sulfate sodium (DSS)-induced model of ulcerative colitis was used to study the function of endogenous galectin-1 during the development of intestinal inflammation. We found that galectin-1 deficient mice (Lgals1−/−mice) displayed a more severe intestinal inflammation, characterized by significantly elevated clinical scores, than their wild type counterparts. The mechanisms underlying the enhanced inflammatory response in coliticLgals1−/−mice involved an altered Th17/Th1 profile of effector CD4+T cells. Furthermore, increased frequencies of Foxp3+CD4+regulatory T cells in colon lamina propria inLgals1−/−mice were found. Strikingly, the exacerbated intestinal inflammatory response observed inLgals1−/−mice was alleviated by adoptive transfer of wild type Foxp3+CD4+regulatory T cells at induction of colitis. Altogether, these data highlight the importance of endogenous galectin-1 as a novel determinant in regulating T cell reactivity during the development of intestinal inflammation.Ministerio de Ciencia, Innovación y Universidades (España)European CommissionDepto. de Biología CelularFac. de Ciencias BiológicasTRUEpubPagado por el auto