4 research outputs found

    Marie-Claire / dir. Jean Prouvost

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    15 janvier 19441944/01/15 (A0,N304)-1944/01/15.Appartient à l’ensemble documentaire : UnivJeun

    Additional file 2: Figure. S1. of Surfen, a proteoglycan binding agent, reduces inflammation but inhibits remyelination in murine models of Multiple Sclerosis

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    a,b. Surfen affects viability of cultured bone marrow derived macrophages (BMDMs) at higher doses (a as assessed by 7-ADD staining, b as assessed by MTT assay, doses indicated). c. Surfen (5 μM) binding to BMDMs is reduced by co-application of heparitinase-III and chondroitinase ABC, alone or in combination. Data is shown as mean ± SEM from 4 independent experiments. Significance compares surfen with vehicle unless otherwise indicated by cross bars (* = P < 0.05) (TIFF 1367 kb

    DataSheet_2_After virus exposure, early bystander naïve CD8 T cell activation relies on NAD+ salvage metabolism.docx

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    CD8 T cells play a central role in antiviral immunity. Type I interferons are among the earliest responders after virus exposure and can cause extensive reprogramming and antigen-independent bystander activation of CD8 T cells. Although bystander activation of pre-existing memory CD8 T cells is known to play an important role in host defense and immunopathology, its impact on naïve CD8 T cells remains underappreciated. Here we report that exposure to reovirus, both in vitro or in vivo, promotes bystander activation of naïve CD8 T cells within 24 hours and that this distinct subtype of CD8 T cell displays an innate, antiviral, type I interferon sensitized signature. The induction of bystander naïve CD8 T cells is STAT1 dependent and regulated through nicotinamide phosphoribosyl transferase (NAMPT)-mediated enzymatic actions within NAD+ salvage metabolic biosynthesis. These findings identify a novel aspect of CD8 T cell activation following virus infection with implications for human health and physiology.</p

    DataSheet_1_After virus exposure, early bystander naïve CD8 T cell activation relies on NAD+ salvage metabolism.pdf

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    CD8 T cells play a central role in antiviral immunity. Type I interferons are among the earliest responders after virus exposure and can cause extensive reprogramming and antigen-independent bystander activation of CD8 T cells. Although bystander activation of pre-existing memory CD8 T cells is known to play an important role in host defense and immunopathology, its impact on naïve CD8 T cells remains underappreciated. Here we report that exposure to reovirus, both in vitro or in vivo, promotes bystander activation of naïve CD8 T cells within 24 hours and that this distinct subtype of CD8 T cell displays an innate, antiviral, type I interferon sensitized signature. The induction of bystander naïve CD8 T cells is STAT1 dependent and regulated through nicotinamide phosphoribosyl transferase (NAMPT)-mediated enzymatic actions within NAD+ salvage metabolic biosynthesis. These findings identify a novel aspect of CD8 T cell activation following virus infection with implications for human health and physiology.</p
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