789 research outputs found
Morphosyntactic Reorganization Phenomena in Arbëresh Dialects: The Neuter
Italo-Albanian communities show different degrees of mixing between Arbëresh, the local Albanian dialect, and the Romance variety in contact. In some Arbëresh dialects the mixing is extensive, affecting lexicon, morpho-syntax and phonology. Contact and bilingualism favour changes in the internal organization of the grammar, as generally in the creolization processes (Savoia 2010; Manzini and Savoia 2015; Baldi and Savoia 2016). This contribution addresses the so-called neuter inflection that Arbëresh dialects spoken in Southern Italian communities preserve, an inflection no longer surviving in standard and other varieties of Albanian, where masculine morphology has replaced it. The coincidence between the specialized -t neuter inflection in nominative and accusative and the plural inflection -t characterizing North-Calabrian Arbëresh led Manzini and Savoia (2017a, 2017b, forthcoming) to connect this morphology with the interpretive properties associated to mass denotation. We hold on to this proposal that has the merit to explain the relation between plural and mass properties. In North-Lucanian and Apulian Arbëresh systems this sub-set of nouns, while maintaining the inflection -t, agrees in feminine. This result can be understood as a consequence of the reorganization that affected these partially mixed grammars, where the original morpho-syntactic mechanisms have been lost or modifie
SPOTS: signaling protein oligomeric transduction structures are early mediators of death receptor–induced apoptosis at the plasma membrane
Fas (CD95, APO-1, TNFRSF6) is a TNF receptor superfamily member that directly triggers apoptosis and contributes to the maintenance of lymphocyte homeostasis and prevention of autoimmunity. Although FADD and caspase-8 have been identified as key intracellular mediators of Fas signaling, it is not clear how recruitment of these proteins to the Fas death domain leads to activation of caspase-8 in the receptor signaling complex. We have used high-resolution confocal microscopy and live cell imaging to study the sequelae of early events in Fas signaling. These studies have revealed a new stage of Fas signaling in which receptor ligation leads to the formation of surface receptor oligomers that we term signaling protein oligomerization transduction structures (SPOTS). Formation of SPOTS depends on the presence of an intact Fas death domain and FADD but is independent of caspase activity. Analysis of cells expressing Fas mutations from patients with the autoimmune lymphoproliferative syndrome (ALPS) reveals that formation of SPOTS can be disrupted by distinct mechanisms in ALPS
Monocytes regulate the mechanism of T-cell death by inducing Fas-mediated apoptosis during bacterial infection.
Monocytes and T-cells are critical to the host response to acute bacterial infection but monocytes are primarily viewed as amplifying the inflammatory signal. The mechanisms of cell death regulating T-cell numbers at sites of infection are incompletely characterized. T-cell death in cultures of peripheral blood mononuclear cells (PBMC) showed 'classic' features of apoptosis following exposure to pneumococci. Conversely, purified CD3(+) T-cells cultured with pneumococci demonstrated necrosis with membrane permeabilization. The death of purified CD3(+) T-cells was not inhibited by necrostatin, but required the bacterial toxin pneumolysin. Apoptosis of CD3(+) T-cells in PBMC cultures required 'classical' CD14(+) monocytes, which enhanced T-cell activation. CD3(+) T-cell death was enhanced in HIV-seropositive individuals. Monocyte-mediated CD3(+) T-cell apoptotic death was Fas-dependent both in vitro and in vivo. In the early stages of the T-cell dependent host response to pneumococci reduced Fas ligand mediated T-cell apoptosis was associated with decreased bacterial clearance in the lung and increased bacteremia. In summary monocytes converted pathogen-associated necrosis into Fas-dependent apoptosis and regulated levels of activated T-cells at sites of acute bacterial infection. These changes were associated with enhanced bacterial clearance in the lung and reduced levels of invasive pneumococcal disease
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