Immunology in the clinic review series. Focus on type 1 diabetes and virus: enterovirus, thymus and type 1 diabetes pathogenesis
; ; et al
in Clinical & Experimental Immunology (2012), 168
Thymus dysfunction, especially immune suppression, is frequently associated with various virus infections.Whether viruses may disturb the thymus function and play a role in the pathogenesis of autoimmune ... [more ▼]
Thymus dysfunction, especially immune suppression, is frequently associated with various virus infections.Whether viruses may disturb the thymus function and play a role in the pathogenesis of autoimmune diseases is an open issue. Enteroviruses, especially Coxsackievirus B4 (CV-B4), have been largely suggested as potential inducers or aggravating factors of type 1 diabetes (T1D) pathogenesis in genetically predisposed individuals. Several pathogenic mechanisms of enterovirus-induced T1D have been suggested. One of these mechanisms is the impairment of central self-tolerance due to viral infections. Coxsackievirus-B4 is able to infect murine thymus in vitro and in vivo and to infect human thymus in vitro. Thymic epithelial cells and thymocytes are targets of infection with this virus, and several abnormalities, especially disturbance of maturation/differentiation processes, were observed.Altogether, these data suggest that CV-B infection of thymus may be involved in the pathogenesis of T1D. Further investigations are needed to explore this hypothesis. [less ▲]Detailed reference viewed: 42 (5 ULg)
Anomalie rénale de l'excrétion sodée, un marqueur de la prédisposition héréditaire à l'hypertension artérielle, rôle de la dopamine?
Krzesinski, Jean-Marie ; ; et al
in Archives des Maladies du Coeur et des Vaisseaux (1989), 82(7), 1245-1248
Since Dahl's observation, a renal defect os sodium excretion is proposed as one of pathogenetic mechanism of hypertension (HTA). Our study has tried to verify this concept in 20 young normotensives with ... [more ▼]
Since Dahl's observation, a renal defect os sodium excretion is proposed as one of pathogenetic mechanism of hypertension (HTA). Our study has tried to verify this concept in 20 young normotensives with (n = 12) and without (n = 8) familial predisposition to HTA, allowing to test the genetic transmission of such potential renal abnormality of sodium balance. Each people was submitted to 3 different Na diet (20, 170 and 340 mM NaCl) each for 1 week. At each visit, blood pressure, vascular resistances, biological values were determined at rest (plasma renin activity, creatinine clearance, 24 hours before the test, catecholamines, aldosterone and ion urinary excretion). Then 1 liter of isotonic saline was perfused in 30 minutes with measures of blood pressure and 3 hours urinary dopamine and Na excretion. During the low and medium Na diets, but not during the high Na diet, the natriuresis and dopamine excretion were lower in the 3 hour urine collection in patients with a family history of HTA (p less than 0.02 and p less than 0.005, respectively). No other clinical or biological difference was noted between the 2 groups. Thus, genetic hypertensive predisposition seems to be characterized by a lower Na excretion during acute Na loading in normal or depleted Na diet, linked to an impaired urinary dopamine excretion. These findings suggest that the defect responsible for the susceptibility to sodium intake is at the kidney level. Some dopamine agonists would be of great therapeutical value in treating such patients when blood pressure begins to rise. [less ▲]Detailed reference viewed: 38 (0 ULg)
Is a renal abnormality of sodium excretion the marker of genetic predisposition to hypertension?
Krzesinski, Jean-Marie ; ; et al
in Clinical & Experimental Hypertension (1989), A11(7), 1391Detailed reference viewed: 7 (0 ULg)