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  • 1
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    Cross-Desensitization of CCR1, but Not CCR2, following Activation of the Formyl Peptide Receptor FPR1 [INNATE IMMUNITY AND INFLAMMATION] (2014)
    The American Association of Immunologists (AAI)
    Details
    Publication Date: 2014-05-17
    Description: The cross-regulation of G protein–coupled receptors (GPCRs) plays an important role in the immune response. Studies from several laboratories have suggested that a hierarchy of sensitivities to cross-desensitization exists for the chemoattractant GPCRs. We carried out experiments to study the capacity of the formyl peptide receptor-1 (FPR1) to desensitize chemokine receptors CCR1 and CCR2. Our results show that activation of FPR1 resulted in the desensitization and partial internalization of CCR1, but not CCR2, in both primary human monocytes and HEK293 cells coexpressing CCR1, CCR2, and FPR1 (HR1R2F cells). The desensitization of CCR1 by FPR1 stimulation was not due to the simple depletion of the Ca 2+ stores, but was dependent on activation of protein kinase C. Furthermore, we found that the cross-desensitization of CCR1 by FPR1 was associated with CCR1 phosphorylation and moderate reduction of CCR1 cell-surface expression. In contrast, CCR2 was not phosphorylated or internalized after FPR1 activation. Additional studies showed that optimal cross talk between FPR1 and CCR1 was dependent on the functional activity of protein kinase Cβ. These results provide a mechanistic basis for the capacity of certain GPCR ligands to exert rapid and selective cross-inactivation of other chemoattractant receptors, and suggest that FPR1 is able to exert "traffic control" in the migration of inflammatory cells by rapidly inhibiting the cell responses to potentially "low-priority" chemoattractants such as CCR1 agonists without inhibiting the response to "higher priority" CCR2 chemoattractants.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
    Published by The American Association of Immunologists (AAI)
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  • 2
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    Dietary Salt Exacerbates Experimental Colitis [INNATE IMMUNITY AND INFLAMMATION] (2017)
    The American Association of Immunologists (AAI)
    Details
    Publication Date: 2017-07-25
    Description: The Western diet is characterized by high protein, sugar, fat, and low fiber intake, and is widely believed to contribute to the incidence and pathogenesis of inflammatory bowel disease (IBD). However, high sodium chloride salt content, a defining feature of processed foods, has not been considered as a possible environmental factor that might drive IBD. We set out to bridge this gap. We examined murine models of colitis on either a high salt diet (HSD) or a low salt diet. We demonstrate that an HSD exacerbates inflammatory pathology in the IL-10–deficient murine model of colitis relative to mice fed a low salt diet. This was correlated with enhanced expression of numerous proinflammatory cytokines. Surprisingly, sodium accumulated in the colons of mice on an HSD, suggesting a direct effect of salt within the colon. Similar to the IL-10–deficient model, an HSD also enhanced cytokine expression during infection by Salmonella typhimurium . This occurred in the first 3 d of infection, suggesting that an HSD potentiates an innate immune response. Indeed, in cultured dendritic cells we found that high salt media potentiates cytokine expression downstream of TLR4 activation via p38 MAPK and SGK1. A third common colitis model, administration of dextran sodium sulfate, was hopelessly confounded by the high sodium content of the dextran sodium sulfate. Our results raise the possibility that high dietary salt is an environmental factor that drives increased inflammation in IBD.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
    Published by The American Association of Immunologists (AAI)
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  • 3
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    Spectroscopy of Surface-Induced Noise Using Shallow Spins in Diamond (2015)
    American Physical Society (APS)
    Details
    Publication Date: 2015-01-07
    Description: Author(s): Y. Romach, C. Müller, T. Unden, L. J. Rogers, T. Isoda, K. M. Itoh, M. Markham, A. Stacey, J. Meijer, S. Pezzagna, B. Naydenov, L. P. McGuinness, N. Bar-Gill, and F. Jelezko We report on the noise spectrum experienced by few nanometer deep nitrogen-vacancy centers in diamond as a function of depth, surface coating, magnetic field and temperature. Analysis reveals a double-Lorentzian noise spectrum consistent with a surface electronic spin bath in the low frequency regim... [Phys. Rev. Lett. 114, 017601] Published Tue Jan 06, 2015
    Keywords: Condensed Matter: Electronic Properties, etc.
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
    Published by American Physical Society (APS)
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  • 4
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    Indistinguishable Photons from Separated Silicon-Vacancy Centers in Diamond (2014)
    American Physical Society (APS)
    Details
    Publication Date: 2014-09-12
    Description: Author(s): A. Sipahigil, K. D. Jahnke, L. J. Rogers, T. Teraji, J. Isoya, A. S. Zibrov, F. Jelezko, and M. D. Lukin Two silicon-vacancy centers in diamond can emit photons that are indistinguishable—suggesting they have potential as building blocks for a diamond-based quantum computer. [Phys. Rev. Lett. 113, 113602] Published Thu Sep 11, 2014
    Keywords: Atomic, Molecular, and Optical Physics
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
    Published by American Physical Society (APS)
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  • 5
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    Candida albicans Stimulates IL-23 Release by Human Dendritic Cells and Downstream IL-17 Secretion by V{delta}1 T Cells [INFECTIOUS DISEASE AND HOST RESPONSE] (2015)
    The American Association of Immunologists (AAI)
    Details
    Publication Date: 2015-06-06
    Description: T cells expressing the V1 TCR are expanded in patients with HIV infection. We show in this article that circulating V1 T cell numbers are particularly high in patients with HIV and candidiasis, and that these cells expand and produce IL-17 in response to Candida albicans in vitro. Although C. albicans could directly stimulate IL-17 production by a subset of V1 T cells, fungus-treated dendritic cells (DCs) were required to expand C. albicans –responsive V1 T cells to generate sufficient numbers of cells to release IL-17 at levels detectable by ELISA. C. albicans induced the release of IL-1β, IL-6, and IL-23 by DCs, but addition of these cytokines or supernatants of C. albicans –treated DCs to V1 T cells was not sufficient to induce proliferation. We found that direct contact with DCs was required for V1 T cell proliferation, whereas IL-23R–blocking studies showed that IL-23 was required for optimal C. albicans –induced IL-17 production. Because IL-17 affords protection against both HIV and C. albicans , and because V1 T cells are not depleted by HIV, these cells are likely to be an important source of IL-17 in HIV-infected patients with candidiasis, in whom CD4 + Th17 responses are impaired. These data show that C. albicans stimulates proliferation and IL-17 production by V1 T cells by a mechanism that involves IL-23 release by DCs.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
    Published by The American Association of Immunologists (AAI)
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