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  • Resultat 111281-111290 av 214685
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111281.
  • Leffler, Jonatan, et al. (författare)
  • Annexin-II, DNA and histones serve as Factor H ligands on the surface of apoptotic cells.
  • 2010
  • Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 285:6, s. 3766-3776
  • Tidskriftsartikel (refereegranskat)abstract
    • Apoptotic cells are opsonized by complement components such as C1q and C3b, which increases their susceptibility to phagocytosis. Soluble complement inhibitors such as factor H (fH)b also recognise apoptotic cells to minimize the pro-inflammatory effects of downstream complement activation. We used four radiolabelled protein constructs that span different regions of the 20 CCP modules that make up fH, and found that fragments comprising CCPs 6-8, CCPs 8-15 and CCPs 19-20 but not CCPs 1-4, bound to apoptotic Jurkat T-cells. There are four possible ligand types on apoptotic cells that could recruit fH: proteins, carbohydrates, lipids and DNA. We found that CCPs 6-8 of fH bind to annexin-II, a trypsin-insensitive protein that becomes exposed on surfaces of apoptotic cells. The second ligand of fH, which interacts with CCPs 6-8 and 19-20, is DNA. Confocal microscopy showed co-localisation of fH with antibodies specific for DNA. FH also binds to histones devoid of DNA and CCPs 1-4, 6-8 and 8-15 mediate this interaction. Treatment of apoptotic cells with neuraminidase, chondroitinase, heparitinase and heparinase did not change fH-binding. Treatment of apoptotic cells with phospholipase A2 dramatically increased both binding of fH and cell-surface DNA. We also excluded the possibility that fH interacts with lysophospholipids using surface plasmon resonance and flow cytometry with lipid-coated beads. Identification of annexin-II as one of the fH ligands on apoptotic cells together with the fact that autoantibodies against annexin-II are found in systemic lupus erythematosus provides further insight into understanding of the pathogenesis of this disease.
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111282.
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111283.
  • Leffler, Jonatan (författare)
  • Complement in Autoimmunity - the importance of clearing waste
  • 2013
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Systemic lupus erythematosus (SLE) is an autoimmune disease where improperly cleared apoptotic cells and neutrophil extracellular traps (NETs) induce an autoimmune response. Complement is crucial to prevent SLE by tailoring immune responses and opsonizing dead cells but may also induce inflammation and tissue damage once the disease is initiated. Complement C1q binds to apoptotic cells and ensures rapid and tolerogenic clearance by phagocytes. C1q can also activate complement. To avoid excessive activation, binding of the complement inhibitor factor H to the apoptotic cells is crucial. In this thesis we have discovered that factor H as well as C1q bind to the phospholipid binding proteins annexin A2 and that C1q also binds A5. These proteins are expressed on apoptotic cells. Further, we have observed that both C1q and factor H bind to the chromatin constituents, DNA and histones. Binding of C1q to these ligands led to complement activation indicating the need for factor H on the apoptotic cells. NETs constitute one mechanism of how neutrophils can protect the body from pathogens. By releasing chromatin covered with antimicrobial enzymes the neutrophil can catch and kill pathogens. In this thesis we confirm that NETs are not degraded properly in 30% of patients with SLE. Further, C1q binds to NETs, prevents degradation and also activates complement. Consequently, the patients with decreased ability to degrade NETs more often suffer from complement consumption and glomerulonephritis, manifestations of severe SLE. This initial study was followed-up by a longitudinal study where temporal associations such as glomerulonephritis, pleuritis and elevated levels of histone antibodies could then be linked to a decreased ability to degrade NETs. NET degradation was also affected in some patients with antiphospholipid syndrome and systemic sclerosis. However the effect was not as pronounced as in SLE and was more evident the more SLE-like the APS was. In conclusion, complement may both prevent and contribute to the pathogenesis in SLE. In this thesis, ligands for complement C1q and factor H have been revealed on the apoptotic cells and further, the interactions of complement with NETs have been elucidated. Additionally, the ability to degrade NETs has been analyzed in SLE and SLE like diseases, which may be used to better diagnose or treat these patients in the future.
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111284.
  • Leffler, Joen (författare)
  • Curation and Reuse : An Experimental Study of Transverse Arrowheads of the Late Scandinavian Mesolithic
  • 2020
  • Ingår i: Lund Archaeological Review. - 1401-2189. ; 24-25, s. 53-61
  • Tidskriftsartikel (refereegranskat)abstract
    • This article aims to examine whether it is possible to rework transversearrowheads while still hafted, in order to reuse them. Three series, eachcontaining three arrows, were shot into a target consisting of meat andbone. When possible, the arrowheads were retouched and fired again.The results of the experiments demonstrate that it is possible to reworktransverse arrowheads while they are hafted and that there may be strongstrategic and economic reasons to do so. A discussion of the results andcomparison with archaeological material follows the experiment, whichindicates that reworked arrowheads can be recognized in archaeologicalcontexts and that reworking changes arrowhead morphology. Thissuggests that formal typologies of lithic arrowheads that are based onmorpho-metric shape, and have been considered to reveal chronologicalor cultural affinities, may be flawed.
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111285.
  • Leffler, Jonatan, et al. (författare)
  • Decreased Neutrophil Extracellular Trap Degradation in Shiga Toxin-Associated Haemolytic Uraemic Syndrome
  • 2017
  • Ingår i: Journal of Innate Immunity. - : S. Karger AG. - 1662-811X .- 1662-8128. ; 9:1, s. 12-21
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Neutrophil extracellular traps (NETs) can stimulate thrombosis, and their degradation is decreased in several autoimmune disorders. It was recently reported that some patients with haemolytic uraemic syndrome (HUS) also fail to degrade NETs and that neutrophils from Shiga toxin-associated HUS are primed to form NETs. Method: We used a well-characterized cohort of 74 thrombotic microangiopathy (TMA) patients, with a subset also providing follow-up samples, and 112 age-matched controls to investigate NET degradation and serum nuclease activity in TMA before, during and after treatment. Results: We identified that in the cohort of TMA patients, 50% of patients with Shiga toxin-associated HUS displayed a decreased ability to degrade NETs. NET degradation correlated with serum nuclease activity, but not with autoantibodies against double-stranded DNA, which has been previously observed in some autoimmune disorders. Further, NET degradation negatively correlated with serum creatinine levels, suggesting that kidney function was negatively impacted by the low NET degradation ability. Conclusions: We revealed that decreased NET degradation is a common feature of Shiga toxin-associated HUS and that it is associated with decreased kidney function in these patients. It remains to be clarified whether improving NET degradation would be beneficial for the patient.
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111286.
  • Leffler, Jonatan, et al. (författare)
  • Degradation of neutrophil extracellular traps co-varies with disease activity in patients with systemic lupus erythematosus
  • 2013
  • Ingår i: Arthritis Research and Therapy. - : Springer Science and Business Media LLC. - 1478-6354. ; 15:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: The ability to degrade neutrophil extracellular traps (NETs) is reduced in a subset of patients with systemic lupus erythematosus (SLE). NETs consist of chromatin covered with antimicrobial enzymes and are normally degraded by DNase-I, an enzyme which is known to have reduced activity in SLE. Decreased ability to degrade NETs is associated with disease activity. In the current study we investigated how the ability of serum from SLE patients to degrade NETs varies during the course of SLE as well as what impact this may have for the clinical phenotype of SLE.Methods: Serum from 69 patients with SLE, included in a prospective study, was taken every 60 days for a median of 784 days. The ability of serum to degrade NETs was determined and associated with clinical parameters occurring before and at the time of sampling, as well as after sampling by using conditional logistic regression.Results: As many as 41% of all patients in the study showed decreased ability to degrade NETs at least once, but with a median of 20% of all time points. Decreased degradation was associated with manifestations of glomerulonephritis as well as low complement levels and elevated levels of antibodies directed against histones and DNA. Furthermore, the odds ratio for the patient to develop alopecia and fever after an episode of decreased NETs degradation was increased by four to five times compared to normal.Conclusions: Decreased degradation of NETs is associated with clinical manifestations in SLE and may contribute to disease pathogenesis. Potential therapeutics restoring the ability to degrade NETs could be beneficial for certain patients with SLE.
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111287.
  • Leffler, Jonatan, et al. (författare)
  • Degradation of neutrophil extracellular traps is decreased in patients with antiphospholipid syndrome.
  • 2014
  • Ingår i: Clinical and Experimental Rheumatology. - 1593-098X. ; 32:1, s. 66-70
  • Tidskriftsartikel (refereegranskat)abstract
    • A decreased ability to degrade neutrophil extracellular traps (NETs) is seen in a subgroup of patients with systemic lupus erythematosus (SLE) and correlates with the presence of autoantibodies. Antiphospholipid syndrome (APS) can develop secondary to SLE or as a primary disease. In the current study we investigated the ability of sera from patients with APS to degrade NETs. The presence of antibodies against NETs and neutrophil remnants were also determined in the same patients.
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111288.
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111289.
  • Leffler, Joen (författare)
  • Jonstorp M2/M3 and Lake Ringsjön Na - different assemblages of archaeological material and perceptions of the Pitted Ware Culture in Scania, Southern Sweden
  • 2015
  • Ingår i: Lund Archaeological Review. - 1401-2189. ; 21, s. 39-47
  • Tidskriftsartikel (refereegranskat)abstract
    • The main aims and goals of this article are to present two assemblages of the Pitted Ware Culture (PWC) in the province of Scania, southern Sweden. One comes from an inland site named Na, located on the northern shore of Lake Ringsjön. Na was excavated in the 1880s. The other site, Jonstorp, is located in north-western Scania and is a coastal site. The sites have historically been connected by a river, Bråån, which makes them good subjects for studying to the use of inland and coastal sites of the PWC. Much of the economy of the sites complement each other, even though there are some differences in hunting, lithic technology and pottery. The secondary aim of this article is to present how archaeological as-semblages can be perceived in different ways due to statistics. During my work with this article I discovered quantities of formerly unknown material from the Na site, changing the statistics. This is also true regarding Jonstorp. The large assemblage excavated in the 1970s is included here, which alters the known statistics. The problem is illustrated using projectile points as an example.
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111290.
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