Correlation between clinical presentation and delayed-enhancement MRI pattern in myocarditis

PURPOSE: The exact incidence of myocarditis is unknown, as the diagnosis is frequently delayed or missed. Clinical presentation and disease course are extremely variable, as there may be acute onset with acute coronary syndrome, or cardiogenic shock, or progressive heart failure or arrhythmias. The purpose of this study was to identify prognostic factors on magnetic resonance imaging (MRI) performed in patients with bioptically proven myocarditis at presentation and after 6 months. MATERIALS AND METHODS: Fifty-six consecutive patients with different presentations of myocarditis (20 with acute coronary syndrome, 20 with heart failure, 16 with arrhythmias) were enrolled. All patients underwent B-mode echocardiography (echo) and tissue Doppler imaging, coronarography, ventriculography, endomyocardial biopsy and contrast-enhanced MRI examination, as well as clinical and echo follow-up at 6 months. RESULTS: At 6-month follow-up, patients were divided in two groups according to values of end-systolic volume and ejection fraction: patients with negative remodelling and those with positive remodelling. Late enhancement was found to be an independent predictor of negative remodelling. CONCLUSIONS: Contrast-enhanced MRI is useful both in the diagnosis and as a prognostic indicator in the clinical suspicion of myocarditis

Non-redundant functions of group 2 innate lymphoid cells

Protective immunity relies on the interplay of innate and adaptive immune cells with complementary and redundant functions. Innate lymphoid cells (ILCs) have recently emerged as tissue-resident, innate mirror images of the T cell system, with which they share lineage-specifying transcription factors and effector machinery. Located at barrier surfaces, ILCs are among the first responders against invading pathogens and thus could potentially determine the outcome of the immune response. However, so far it has not been possible to dissect the unique contributions of ILCs to protective immunity owing to limitations in specific targeting of ILC subsets. Thus, all of the available data have been generated either in mice lacking the adaptive immune system or with tools that also affect other immune cell subsets. In addition, it has been proposed that ILCs might be dispensable for a proper immune response because other immune cells could compensate for their absence. Here we report the generation of a mouse model based on the neuromedin U receptor 1 (Nmur1) promoter as a driver for simultaneous expression of Cre recombinase and green fluorescent protein, which enables gene targeting in group 2 ILCs (ILC2s) without affecting other innate and adaptive immune cells. Using Cre-mediated gene deletion of Id2 and Gata3 in Nmur1-expressing cells, we generated mice with a selective and specific deficiency in ILC2s. ILC2-deficient mice have decreased eosinophil counts at steady state and are unable to recruit eosinophils to the airways in models of allergic asthma. Further, ILC2-deficient mice do not mount an appropriate immune and epithelial type 2 response, resulting in a profound defect in worm expulsion and a non-protective type 3 immune response. In total, our data establish non-redundant functions for ILC2s in the presence of adaptive immune cells at steady state and during disease and argue for a multilayered organization of the immune system on the basis of a spatiotemporal division of labour