4 research outputs found
Des vestiges de consommation de sel sur le site laténien de Brebières « Les Béliers » (Pas-de-Calais)
International audienc
Des vestiges de consommation de sel sur le site laténien de Brebières « Les Béliers » (Pas-de-Calais)
International audienceLe site de Brebières « Les Béliers » (Pas-de-Calais) a fait l'objet d'une opération de diagnostic couvrant une surface de 60 ha aboutissant à la fouille d'une superficie de 17 ha. Celle-ci a donné lieu à la découverte d'une vingtaine d'enclos fossoyés dont la datation s'échelonne de La Tène C à La Tène D. Près de 2 000 fragments de moules à sel, pour un poids d'environ 6 kg, ont été mis au jour. Implanté à une centaine de kilomètres des côtes et à une vingtaine de kilomètres d'Arras (fig. 1), l'absence de toute trace d'artisanat du sel exclut cependant la possibilité d'un atelier de saunier. Ce site constitue l'un des principaux témoins de la consommation de sel dans le Nord de la France
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Patients with Type 1 Diabetes Display Selective Defect in Antigen Receptor Mediated T Cell Apoptosis
Type 1 diabetes is an autoimmune disease in which insulin-producing beta cells are destroyed by auto-reactive T lymphocytes. Studies in mice indicate that incomplete deletion of self-reactive T-cells and compromised peripheral tolerance mechanisms can contribute to the manifestation of autoimmune diabetes. In patients with type 1 diabetes, defects in T regulatory cell numbers and function have been previously reported. In this study, we have ascertained the integrity of activation-induced cell death, a mechanism of peripheral T cell tolerance, in long-standing type 1 diabetes patients. Activation of peripheral blood derived T cells from non-diabetic individuals with a T cell mitogen and interleukin-2 rendered them susceptible to subsequent T-cell receptor/CD3mediated apoptosis, as indicated by the dissipation of the mitochondrial membrane potential and activation of intracellular caspases. In contrast, similarly activated T lymphocytes from type 1 diabetes patients failed to undergo apoptosis when challenged with a bacterial superantigen or anti-CD3 antibody. Supplementation of T cell cultures with interleukin-4 or interleukin-18 failed to restore self-tolerance. However, both the expression of the Fas receptor and its ability to transduce apoptotic signal were comparable in T cells of type 1 diabetes patients and controls. Additionally, no marked difference in the T cell subsets was observed between controls and diabetes patients under all activation conditions analyzed. These data suggest that the abnormality in T-cell receptor-mediated apoptosis is cell autonomous in long-standing type 1 diabetes patients, which in addition to other defective peripheral tolerance mechanisms, likely to contribute to the manifestation of autoimmune diabetes