280 research outputs found

    Respiratory syncytial virus infection modifies and accelerates pulmonary disease via DC activation and migration

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141386/1/jlb0005.pd

    Regulation of Immunity to Respiratory Syncytial Virus by Dendritic Cells, Toll-Like Receptors, and Notch

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    The activation and maintenance of pulmonary viral disease is regulated at multiple levels and determined by the early innate response to the pathogenic stimuli. Subsequent activation events that rely directly and indirectly on the virus itself can alter the development and severity of the ensuing immunopathologic responses. In the present review we outline several interconnected mechanisms that rely on the early recognition of viral nucleic acid for the most appropriate anti-viral immune responses, including TLRs and Notch activation in DCs and T cells. Deviation or persistence of the immune response to respiratory viruses may impact significantly on the severity of the responses. While these mechanisms are likely similar in most respiratory viral infections, this review will focus on findings with respiratory syncytial virus (RSV) infections.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/63262/1/vim.2007.0110.pd

    A Gene Network Perspective on Axonal Regeneration

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    The regenerative capacity of injured neurons in the central nervous system is limited due to the absence of a robust neuron-intrinsic injury-induced gene response that supports axon regeneration. In peripheral neurons axotomy induces a large cohort of regeneration-associated genes (RAGs). The forced expression of some of these RAGs in injured neurons has some beneficial effect on axon regeneration, but the reported effects are rather small. Transcription factors (TFs) provide a promising class of RAGs. TFs are hubs in the regeneration-associated gene network, and potentially control the coordinate expression of many RAGs simultaneously. Here we discuss the use of combined experimental and computational methods to identify novel regeneration-associated TFs with a key role in initiating and maintaining the RAG-response in injured neurons. We propose that a relatively small number of hub TFs with multiple functional connections in the RAG network might provide attractive new targets for gene-based and/or pharmacological approaches to promote axon regeneration in the central nervous system

    Adhesive bonding of InP/InGaAsP dies to processed silicon-on-insulator wafers using DVS-bis-benzocyclobutene

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    The process of bonding InP/InGaAsP dies to a processed silicon-on-insulator wafer using sub-300 nm layers of DVS-bis-benzocyclobutene (BCB) was developed. The planarization properties of these DVS-bis-BCB layers were measured and an optimal prebonding die preparation and polymer precure are presented. Bonding quality and bonding strength are assessed, showing high-quality bonding with sufficient bonding strength to survive postbonding processing

    The Balance between Plasmacytoid DC versus Conventional DC Determines Pulmonary Immunity to Virus Infections

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    Background: Respiratory syncytial virus (RSV) infects nearly all infants by age 2 and is a leading cause of broncialitis. RSV may employ several mechanisms to induce immune dysregulation, including dentritic cell (DC) modulation during the immune response to RSV. Methods and Findings: Expansion of cDC and pDC by Flt3L treatment promoted an anti-viral response with reduced pathophysiology characterized by decreased airway hyperreactivity, reduced Th2 cytokines, increased Th1 cytokines, and a reduction in airway inflammation and mucus overexpression. These protective aspects of DC expansion could be completely reversed by depleting pDCs during the RSV infections. Expansion of DCs by Flt3L treatment enhanced in CD8+ T cell responses, which was reversed by depletion of pDC. Conclusions: These results indicate that a balance between cDC and pDC in the lung and its lymph nodes is crucial for the outcome of a pulmonary infection. Increased pDC numbers induced by Flt3L treatment have a protective impact on the nature of the overall immune environment
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