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- Kannan, Bharath, et al.
(författare)
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Waveguide quantum electrodynamics with superconducting artificial giant atoms
- 2020
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 583:7818, s. 775-779
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Tidskriftsartikel (refereegranskat)abstract
- Models of light–matter interactions in quantum electrodynamics typically invoke the dipole approximation1,2, in which atoms are treated as point-like objects when compared to the wavelength of the electromagnetic modes with which they interact. However, when the ratio between the size of the atom and the mode wavelength is increased, the dipole approximation no longer holds and the atom is referred to as a ‘giant atom’2,3. So far, experimental studies with solid-state devices in the giant-atom regime have been limited to superconducting qubits that couple to short-wavelength surface acoustic waves4–10, probing the properties of the atom at only a single frequency. Here we use an alternative architecture that realizes a giant atom by coupling small atoms to a waveguide at multiple, but well separated, discrete locations. This system enables tunable atom–waveguide couplings with large on–off ratios3 and a coupling spectrum that can be engineered by the design of the device. We also demonstrate decoherence-free interactions between multiple giant atoms that are mediated by the quasi-continuous spectrum of modes in the waveguide—an effect that is not achievable using small atoms11. These features allow qubits in this architecture to switch between protected and emissive configurations in situ while retaining qubit–qubit interactions, opening up possibilities for high-fidelity quantum simulations and non-classical itinerant photon generation12,13.
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- Lundtoft, Christian, et al.
(författare)
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Function of multiple sclerosis-protective HLA class I alleles revealed by genome-wide protein-quantitative trait loci mapping of interferon signalling
- 2020
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Ingår i: PLOS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 16:10
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Tidskriftsartikel (refereegranskat)abstract
- Interferons (IFNs) are cytokines that are central to the host defence against viruses and other microorganisms. If not properly regulated, IFNs may contribute to the pathogenesis of inflammatory autoimmune, or infectious diseases. To identify genetic polymorphisms regulating the IFN system we performed an unbiased genome-wide protein-quantitative trait loci (pQTL) mapping of cell-type specific type I and type II IFN receptor levels and their responses in immune cells from 303 healthy individuals. Seven genome-wide significant (p < 5.0E-8) pQTLs were identified. Two independent SNPs that tagged the multiple sclerosis (MS)-protective HLA class I alleles A*02/A*68 and B*44, respectively, were associated with increased levels of IFNAR2 in B and T cells, with the most prominent effect in IgD–CD27+ memory B cells. The increased IFNAR2 levels in B cells were replicated in cells from an independent set of healthy individuals and in MS patients. Despite increased IFNAR2 levels, B and T cells carrying the MS-protective alleles displayed a reduced response to type I IFN stimulation. Expression and methylation-QTL analysis demonstrated increased mRNA expression of the pseudogene HLA-J in B cells carrying the MS-protective class I alleles, possibly driven via methylation-dependent transcriptional regulation. Together these data suggest that the MS-protective effects of HLA class I alleles are unrelated to their antigen-presenting function, and propose a previously unappreciated function of type I IFN signalling in B and T cells in MS immune-pathogenesis.Author summaryGenetic association studies have been very successful in identifying disease-associated single nucleotide polymorphisms (SNPs), but it has been challenging to define the molecular mechanisms underlying these associations. As interferons (IFNs) have a central role in the immune system, we hypothesized that some of the SNPs associated to immune-mediated diseases would affect the IFN system. By combining genetic data with characterization of interferon receptor levels and their responses on the protein level in immune cells from 303 genotyped healthy individuals, we show that two SNPs tagging the HLA class I alleles A*02/A*68 and B*44 are associated with a decreased response to type I IFN stimulation in B cells and T cells. Notably, both HLA-A*02 and HLA-B*44 confer protection from developing multiple sclerosis (MS), which is a chronic inflammatory neurologic disease. In addition to suggesting a pathogenic role of enhanced type I interferon signalling in B cells and T cells in MS, our data emphasize the fact that genetic associations in the HLA locus can affect functions not directly associated to antigen presentation, which conceptually may be important for other diseases genetically associated to the HLA locus.
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