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Träfflista för sökning "WFRF:(Persson Alexander 1978 ) srt2:(2010-2014)"

Sökning: WFRF:(Persson Alexander 1978 ) > (2010-2014)

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1.
  • Andersson, Henrik, et al. (författare)
  • Apoptotic neutrophils augment the inflammatory response to Mycobacterium tuberculosis infection in human macrophages
  • 2014
  • Ingår i: PLOS ONE. - : PLOS. - 1932-6203. ; 9:7
  • Tidskriftsartikel (refereegranskat)abstract
    • Macrophages in the lung are the primary cells being infected by Mycobacterium tuberculosis (Mtb) during the initial manifestation of tuberculosis. Since the adaptive immune response to Mtb is delayed, innate immune cells such as macrophages and neutrophils mount the early immune protection against this intracellular pathogen. Neutrophils are short-lived cells and removal of apoptotic cells by resident macrophages is a key event in the resolution of inflammation and tissue repair. Since anti-inflammatory activity is not compatible with effective immunity to intracellular pathogens, we therefore investigated how uptake of apoptotic neutrophils modulates the function of Mtb-activated human macrophages. We show that Mtb infection exerts a potent proinflammatory activation of human macrophages with enhanced gene activation and release of proinflammatory cytokines and that this response was augmented by apoptotic neutrophils. The enhanced macrophage response is linked to apoptotic neutrophil-driven activation of the NLRP3 inflammasome and subsequent IL-1β signalling. We also demonstrate that apoptotic neutrophils not only modulate the inflammatory response, but also enhance the capacity of infected macrophages to control intracellular growth of virulent Mtb. Taken together, these results suggest a novel role for apoptotic neutrophils in the modulation of the macrophage-dependent inflammatory response contributing to the early control of Mtb infection.
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2.
  • Redjai Sani, Sohrab, et al. (författare)
  • Mutually synchronized bottom-up multi-nanocontact spin-torque oscillators
  • 2013
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 4, s. 2731-
  • Tidskriftsartikel (refereegranskat)abstract
    • Spin-torque oscillators offer a unique combination of nanosize, ultrafast modulation rates and ultrawide band signal generation from 100 MHz to close to 100 GHz. However, their low output power and large phase noise still limit their applicability to fundamental studies of spin-transfer torque and magnetodynamic phenomena. A possible solution to both problems is the spin-wave-mediated mutual synchronization of multiple spin-torque oscillators through a shared excited ferromagnetic layer. To date, synchronization of high-frequency spin-torque oscillators has only been achieved for two nanocontacts. As fabrication using expensive top-down lithography processes is not readily available to many groups, attempts to synchronize a large number of nanocontacts have been all but abandoned. Here we present an alternative, simple and cost-effective bottom-up method to realize large ensembles of synchronized nanocontact spin-torque oscillators. We demonstrate mutual synchronization of three high-frequency nanocontact spin-torque oscillators and pairwise synchronization in devices with four and five nanocontacts.
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3.
  • Vanden Driessche, Koen, et al. (författare)
  • Immune vulnerability of infants to tuberculosis
  • 2013
  • Ingår i: Clinical & Developmental Immunology. - : Hindawi Publishing Corporation. - 1740-2522 .- 1740-2530. ; 2013
  • Forskningsöversikt (refereegranskat)abstract
    • One of the challenges faced by the infant immune system is learning to distinguish the myriad of foreign but nonthreatening antigens encountered from those expressed by true pathogens. This balance is reflected in the diminished production of proinflammatory cytokines by both innate and adaptive immune cells in the infant. A downside of this bias is that several factors critical for controlling Mycobacterium tuberculosis infection are significantly restricted in infants, including TNF, IL-1, and IL-12. Furthermore, infant T cells are inherently less capable of differentiating into IFN- γ -producing T cells. As a result, infected infants are 5-10 times more likely than adults to develop active tuberculosis (TB) and have higher rates of severe disseminated disease, including miliary TB and meningitis. Infant TB is a fundamentally different disease than TB in immune competent adults. Immunotherapeutics, therefore, should be specifically evaluated in infants before they are routinely employed to treat TB in this age group. Modalities aimed at reducing inflammation, which may be beneficial for adjunctive therapy of some forms of TB in older children and adults, may be of no benefit or even harmful in infants who manifest much less inflammatory disease.
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