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    Investigation of carboxylated multi-walled carbon nanotube cytotoxicity in vitro : a thesis presented in partial fulfilment of the requirements for the degree of Masters of Science in Physiology at Massey University, Palmerston North, New Zealand
    (Massey University, 2010) Gilmour, Aaron David
    Carbon nanotubes have been idealised as carrier vehicles for cell targeted drug and gene delivery. The physiochemical properties of the carbon nanotube also promote its function as a „thermal antennae‟ for non-invasive cancer destruction. Covalent modification of carbon nanotubes is a result of acidic purification resulting in carboxylated carbon nanotubes. Additionally this covalent modification allows for the attachment of biological moieties for cell targeting. Conversely, carboxylated carbon nanotubes are suggested to be cytotoxic to mammalian cells. The current study investigates the potential cytotoxicity of short, carboxylated, multi-walled carbon nanotubes in vitro, in a primary fibroblast cell culture model. Cytotoxicity is assessed with vital staining using propidium iodide, and secondly with a lactate dehydrogenase colorimetric assay. Results indicate that there is a dose dependent cytotoxic relationship between the carboxylated multi-walled carbon nanotubes tested and the fibroblast cell culture model.
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    Antigen-specific cytotoxic T lymphocytes target airway CD103+ and CD11b+ dendritic cells to suppress allergic inflammation
    (Nature Publishing Group, 2016-01) Daniels NJ; Hyde E; Ghosh S; Seo K; Price KM; Hoshino K; Kaisho T; Okada T; Ronchese F
    Allergic airway inflammation is driven by the recognition of inhaled allergen by T helper type 2 (Th2) cells in the airway and lung. Allergen-specific cytotoxic T lymphocytes (CTLs) can strongly reduce airway inflammation, however, the mechanism of their inhibitory activity is not fully defined. We used mouse models to show that allergen-specific CTLs reduced early cytokine production by Th2 cells in lung, and their subsequent accumulation and production of interleukin (IL)-4 and IL-13. In addition, treatment with specific CTLs also increased the proportion of caspase+ dendritic cells (DCs) in mediastinal lymph node (MLN), and decreased the numbers of CD103+ and CD11b+ DCs in the lung. This decrease required expression of the cytotoxic mediator perforin in CTLs and of the appropriate MHC-antigen ligand on DCs, suggesting that direct CTL-DC contact was necessary. Lastly, lung imaging experiments revealed that in airway-challenged mice XCR1-GFP+ DCs, corresponding to the CD103+ DC subset, and XCR1-GFP− CD11c+ cells, which include CD11b+ DCs and alveolar macrophages, both clustered in the areas surrounding the small airways and were closely associated with allergen-specific CTLs. Thus, allergen-specific CTLs reduce allergic airway inflammation by depleting CD103+ and CD11b+ DC populations in the lung, and may constitute a mechanism through which allergic immune responses are regulated.