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  • 1.
    Barbu, Andreea
    et al.
    Uppsala University.
    Hamad, Osama
    Uppsala University.
    Lind, Lars
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Uppsala University.
    Nilsson, Bo
    Uppsala University.
    The role of complement factor C3 in lipid metabolism2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 101-107Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Abundant reports have shown that there is a strong relationship between C3 and C3a-desArg levels, adipose tissue, and risk factors for cardiovascular disease, metabolic syndrome and diabetes. The data indicate that complement components, particularly C3, are involved in lipid metabolism. The C3 fragment, C3a-desArg, functions as a hormone that has insulin-like effects and facilitates triglyceride metabolism. Adipose tissue produces and regulates the levels of complement components, which promotes generation of inflammatory initiators such as the anaphylatoxins C3a and C5a. The anaphylatoxins trigger a cyto/chemokine response in proportion to the amount of adipose tissue present, and induce inflammation and mediate metabolic effects such as insulin resistance. These observations support the concept that complement is an important participant in lipid metabolism and in obesity, contributing to the metabolic syndrome and to the low-grade inflammation associated with obesity.

  • 2.
    Bergseth, Grethe
    et al.
    Nordland Hospital, Bodø, Norway.
    Nilsson, Per H.
    University of Oslo, Rikshospitalet, Norway.
    Thomas, Anub Mathew
    Radboud University Medical Center, The Netherlands.
    Gustavsen, Alice
    University of Oslo, Rikshospitalet, Norway.
    Volokhina, Elena B
    Radboud University Medical Center, The Netherlands.
    van den Heuvel, Lambertus P
    Radboud University Medical Center, The Netherlands.
    Barratt-Due, Andreas
    University of Oslo, Rikshospitalet, Norway.
    Mollnes, Tom E
    University of Oslo, Rikshospitalet, Norway;Nordland Hospital, Norway;University of Tromsø, Norway.
    Neoepitope based assays to detect C5a – Pitfalls and interpretations2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, nr SI: EMCHD2017, s. 201-201Artikel i tidskrift (Refereegranskat)
  • 3.
    Bexborn, Fredrik
    et al.
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Andersson, Per Ola
    Chen, Hsui
    Nilsson, Bo
    Nilsson Ekdahl, Kristina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    The Tick-Over Theory Revisited: Formation and Regulation of the Soluble Alternative Complement C3 Convertase (C3(H2O)Bb)2008Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 45, nr 8, s. 2370-2379Artikel i tidskrift (Refereegranskat)
  • 4.
    Carlsson, Hanna
    et al.
    Kalmar County Hospital.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Tjernberg, Ivar
    Kalmar County Hospital.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement activation in asymptomatic Lyme borreliosis and neuroborreliosis2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 128-128Artikel i tidskrift (Övrigt vetenskapligt)
  • 5.
    Engberg, Anna E.
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson, Per H.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Univ Oslo, Rikshosp, Univ Hosp, Norway.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Huang, Shan
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Mollnes, T. E.
    Nicholls, Ian A.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala university.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala university.
    The ratio between C4 and C4BP adsorbed to artificial materials is a new predictor for biocompatibility2013Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 56, nr 3, s. 309-309Artikel i tidskrift (Övrigt vetenskapligt)
  • 6.
    Fromell, Karin
    et al.
    Uppsala University.
    Duhrkop, Claudia
    Uppsala University.
    Johansson, Ulrika
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Forms of contact-activated C3 associated with AP convertase formation2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 141-141Artikel i tidskrift (Övrigt vetenskapligt)
  • 7.
    Fromell, Karin
    et al.
    Uppsala Universit.
    Duhrkop, Claudia
    Uppsala University.
    Kozarcanin, Huda
    Uppsala University.
    Johansson, Ulrika
    Uppsala University.
    Skjoedt, Mikkel-Ole
    Rigshosp, Denmark.
    Garred, Peter
    Rigshosp, Denmark.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    The lectin pathway of complement and the contact/kallikrein system are integrated2018Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 102, s. 151-152Artikel i tidskrift (Övrigt vetenskapligt)
  • 8.
    Fromell, Karin
    et al.
    Uppsala University.
    Johansson, Ulrika
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Duhrkop, Claudia
    Uppsala University.
    Adler, Anna
    Uppsala University.
    Usterud, Emma
    Uppsala University.
    Hamad, Osama A.
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Generation of an alternative pathway convertase by contact-activated C3 is dependent on the conformation of C32018Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 102, s. 193-193Artikel i tidskrift (Övrigt vetenskapligt)
  • 9.
    Hamad, Osama
    et al.
    Rudbeck Laboratory, University hospital, Uppsala.
    Nilsson, Per H.
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Lambris, John D.
    University of Pennsylvania, USA.
    Nilsson Ekdahl, Kristina
    Högskolan i Kalmar, Naturvetenskapliga institutionen. Rudbeck Laboratory, University hospital, Uppsala.
    Nilsson, Bo
    Rudbeck Laboratory, University hospital, Uppsala.
    Binding of complement proteins to activated platelets is independent of complement activation2009Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 46, nr 14, s. 2853-2853, artikel-id OP95Artikel i tidskrift (Refereegranskat)
  • 10.
    Harboe, M.
    et al.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway.
    Nilsson, Per H.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway.
    Johnson, C.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway.
    Lindstad, J. K.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway.
    Pharo, A.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway.
    Hellerud, B. C.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway.
    Nymo, S.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway ; University of Tromsö, Norway.
    Mollnes, T. E.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway ; University of Tromsö, Norway.
    Binding of properdin to myeloperoxidase and Neisseria meningitidis is C3-dependent2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, Special Issue, s. 142-142, artikel-id 067Artikel i tidskrift (Refereegranskat)
  • 11.
    Helin, Anu S.
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för biologi och miljö (BOM).
    Wille, Michelle
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för biologi och miljö (BOM).
    Atterby, Clara
    Uppsala University.
    Jarhult, Josef D.
    Uppsala University.
    Waldenström, Jonas
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för biologi och miljö (BOM).
    Chapman, Joanne R.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för biologi och miljö (BOM). Univ Kansas, USA.
    A rapid and transient innate immune response to avian influenza infection in mallards2018Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 95, s. 64-72Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The vertebrate innate immune system provides hosts with a rapid, non-specific response to a wide range of invading pathogens. However, the speed and duration of innate responses will be influenced by the co-evolutionary dynamics of specific host-pathogen combinations. Here, we show that low pathogenic avian influenza virus (LPAI) subtype H1N1 elicits a strong but extremely transient innate immune response in its main wildlife reservoir, the mallard (Anas platyrhynchos). Using a series of experimental and methodological improvements over previous studies, we followed the expression of retinoic acid inducible gene 1 (RIG-I) and myxovirus resistance gene (Mx) in mallards semi-naturally infected with low pathogenic H1N1. One day post infection, both RIG-I and Mx were significantly upregulated in all investigated tissues. By two days post infection, the expression of both genes had generally returned to basal levels, and remained so for the remainder of the experiment. This is despite the fact that birds continued to actively shed viral particles throughout the study period. We additionally show that the spleen plays a particularly active role in the innate immune response to LPAI. Waterfowl and avian influenza viruses have a long co-evolutionary history, suggesting that the mallard innate immune response has evolved to provide a minimum effective response to LPAIs such that the viral infection is brought under control while minimising the damaging effects of a sustained immune response.

  • 12.
    Huang, Shan
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    iC3 generation elicited by the presence of ammonia and urea in human plasma2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 145-145Artikel i tidskrift (Övrigt vetenskapligt)
  • 13.
    Jonsson, Nina
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Asif, Sana
    Uppsala University.
    Teramura, Yuji
    Univ Tokyo, Japan.
    Gustafson, Elisabeth
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Surface modification of primary human hepatocytes with recombinant CD39 protects against thromboinfiammation2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 149-150Artikel i tidskrift (Övrigt vetenskapligt)
  • 14.
    Kozarcanin, Huda
    et al.
    Uppsala University.
    Lood, Christian
    Skåne Univ Hosp, Sweden;Lund Univ, Sweden.
    Munthe-Fog, Lea
    Univ Copenhagen, Denmark.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Hamad, Osama
    Uppsala University.
    Skjoedt, Mikkel-Ole
    Univ Copenhagen, Denmark.
    Bengtsson, Anders
    Skåne Univ Hosp, Sweden;Lund Univ, Sweden.
    Huber-Lang, Markus
    Univ Hosp Ulm, Germany.
    Garred, Peter
    Univ Copenhagen, Denmark.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    The lectin complement pathway serine proteases bridges the complement and the coagulation systems in thrombotic diseases2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 153-153Artikel i tidskrift (Övrigt vetenskapligt)
  • 15.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Johansson, Kjell
    Örebro University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement factor involvement during experimental AMD2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 163-163Artikel i tidskrift (Övrigt vetenskapligt)
  • 16.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Petrus-Reurer, S.
    Karolinska Institutet;Karolinska Univ Hosp.
    Lanner, F.
    Karolinska Institutet;Karolinska Univ Hosp.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Kvanta, A.
    Karolinska Institutet.
    Nilsson, B.
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement system proteins in human embryonic stem cell-derived retinal pigment epithelial cells co-cultured with or without porcine retina2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 162-163Artikel i tidskrift (Övrigt vetenskapligt)
  • 17.
    Mohlin, Camilla
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University, Sweden.
    Nilsson, Bo
    Uppsala University, Sweden.
    The link between morphology and complement in ocular disease2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 84-99Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The complement system is a vital component of the immune-priveliged human eye that is always active at a low-grade level, preventing harmful intraocular injuries caused by accumulation of turnover products and controlling pathogens to preserve eye homeostasis and vision. The complement system is a double-edged sword that is essential for protection but may also become harmful and contribute to eye pathology. Here, we review the evidence for the involvement of complement system dysregulation in age-related macular degeneration, glaucoma, uveitis, and neuromyelitis optica, highlighting the relationship between morphogical changes and complement system protein expression and regulation in these diseases. The potential benefits of complement inhibition in age-related macular degeneration, glaucoma, uveitis, and neuromyelitis optica are abundant, as are those of further research to improve our understanding of complement-mediated injury in these diseases.

  • 18.
    Mollnes, T.
    et al.
    University of Oslo, Norway.
    Baratt-Due, A.
    University of Oslo, Norway.
    Pischke, S.
    Oslo University Hospital, Norway.
    Sandanger, I.
    Oslo University Hospital, Norway.
    Nilsson, Per H.
    University of Oslo, Norway.
    Lambris, J.
    University of Philadelphia, USA.
    Nunn, M.
    Centre for Ecology and Hydrology, Oxford, UK.
    Denk, S.
    University of Ulm, Germany.
    Espevik, T.
    Norwegian University of Science and Technology, Norway.
    Huber-Lang, M.
    University of Ulm, Germany.
    Double-blockade of CD14 and complement component C5 abolish the inflammatory storm and improve survival in mouse polymicrobial sepsis2013Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 56, nr 3, s. 294-294Artikel i tidskrift (Refereegranskat)
  • 19.
    Nilsson, Bo
    et al.
    Uppsala University.
    Asif, Sana
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Manell, Elin
    Swedish University of Agricultural Sciences.
    Biglarnia, Alireza
    Skåne University Hospital.
    Jensen-Waern, Marianne
    Swedish University of Agricultural Sciences.
    Teramura, Yuji
    Uppsala University;Univ Tokyo, Japan.
    A protective role of complement regulators linked to a PEG phospholipid construct in reducing ischemic reperfusion injury in transplantation2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 208-208Artikel i tidskrift (Övrigt vetenskapligt)
  • 20.
    Nilsson, Bo
    et al.
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Uppsala University.
    Kemper, Claudia
    King's College London, UK.
    Mollnes, Tom Eirik
    Nordland Hospital, Norway;University of Tromsø, Norway.
    Preface. 15th European Meeting on Complement in Human Disease 2015, Uppsala, Sweden.2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 1-2Artikel i tidskrift (Övrigt vetenskapligt)
  • 21. Nilsson, Bo
    et al.
    Nilsson Ekdahl, Kristina
    Department of Clinical Immunology and Transfusion Medicine, University Hospital, Uppsala.
    Svensson, K E
    Bjelle, A
    Nilsson, U R
    Distinctive expression of neoantigenic C3(D) epitopes on bound C3 following activation and binding to different target surfaces in normal and pathological human sera1989Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 26, nr 4, s. 383-390Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Binding of C3 to sheep erythrocytes in a serum-free milieu (EAC14oxy2, EAC142) has previously been shown to mimic the antigenic change that occurs upon denaturation of C3 in sodium dodecyl sulphate (SDS), whereby neoantigenic C3(D) epitopes are exposed. The present paper deals with C3 bound to various target surfaces which are known to modulate the functional properties of C3 in different ways. Bound C3 fragments on serum-treated human aggregated gammaglobulin, zymosan, rabbit and sheep erythrocytes, and on circulating immune complexes isolated from sera of patients with rheumatoid arthritis and systemic lupus erythematosus, were shown to be mainly in the iC3b form. By RIAs, employing polyclonal antibodies, the range of C3(D) antigenic epitopes of 125I-labelled SDS denatured C3 expressed by the particle-bound iC3b was monitored. The physiologically bound iC3b on all tested particles expressed wide ranges of C3(D) epitopes and each type of particle-bound C3 exposed its individual range. By competition ELISA specific C3(D)α epitopes were monitored, employing monoclonal antibodies. A distinct difference in the expression of these epitopes was observed in iC3b bound to various test particles in the presence of normal serum and in iC3b present on circulating immune complexes from pathological sera. Considering that the neoantigenic C3(D) epitopes have been shown to be associated with different functions of C3, the distinctive antigenic expression of each type of serum-treated particle might reflect different functional forms of the protein. 

  • 22.
    Nilsson, Bo
    et al.
    Uppsala University.
    Teramura, Yuji
    Uppsala University;University of Tokyo.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    The role and regulation of complement activation as part of the thromboinflammation elicited in cell therapies2014Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 61, nr 2, s. 185-190Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Cell therapies in which the cells come into direct contact with blood and other body fluids are emerging treatment procedures for patients with various diseases, such as diabetes mellitus, liver insufficiency, and graft-versus-host disease. However, despite recent progress, these procedures are associated with tissue loss caused by thromboinflammatory reactions. These deleterious reactions involve the activation of the complement and coagulation cascades and platelet and leukocyte activation, ultimately resulting in clot formation and damage to the implanted cells. In this concept review, we discuss the basic mechanisms underlying the thrombininflammatory process, with special reference to the engagement of complement and emerging strategies for the therapeutic regulation of these reactions that include the use of selective systemic inhibitors and various procedures to coat the surfaces of the cells. The coating procedures may also be applied to other treatment modalities in which similar mechanisms are involved, including whole organ transplantation, treatment with biomaterials in contact with blood, and extracorporeal procedures. (C) 2014 Published by Elsevier Ltd.

  • 23.
    Nilsson Ekdahl, Kristina
    et al.
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Blomberg, Carolina
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Henningsson Johnsson, Anna
    Dahle, Charlotte
    Håkansson, Irene
    Sandholm, Kerstin
    Högskolan i Kalmar, Naturvetenskapliga institutionen.
    Ernerudh, Jan
    Systemic and Intrathecal Complement Activation in Multiple Sclerosis and Guillan-Barré Syndrome2009Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 46, nr 14, s. 2848-2848Artikel i tidskrift (Refereegranskat)
  • 24.
    Nilsson Ekdahl, Kristina
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala university, Sweden.
    Mohlin, Camilla
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Adler, Anna
    Uppsala university, Sweden.
    Aman, Amanda
    Uppsala university, Sweden.
    Manivel, Vivek Anand
    Uppsala university, Sweden.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Huber-Lang, Markus
    Univ Hosp Ulm, Germany.
    Fromell, Karin
    Uppsala university, Sweden.
    Nilsson, Bo
    Uppsala university, Sweden.
    Is generation of C-3(H2O) necessary for activation of the alternative pathway in real life?2019Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 114, s. 353-361Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In the alternative pathway (AP) an amplification loop is formed, which is strictly controlled by various fluid-phase and cell-bound regulators resulting in a state of homeostasis. Generation of the "C3b-like" C3(H2O) has been described as essential for AP activation, since it conveniently explains how the initial fluid-phase AP convertase of the amplification loop is generated. Also, the AP has a status of being an unspecific pathway despite thorough regulation at different surfaces. During complement attack in pathological conditions and inflammation, large amounts of C3b are formed by the classical/lectin pathway (CP/LP) convertases. After the discovery of LP's recognition molecules and its tight interaction with the AP, it is increasingly likely that the AP acts in vivo mainly as a powerful amplification mechanism of complement activation that is triggered by previously generated C3b molecules initiated by the binding of specific recognition molecules. Also in many pathological conditions caused by a dysregulated AP amplification loop such as paroxysmal nocturnal hemoglobulinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), C3b is available due to minute LP and CP activation and/or generated by non-complement proteases. Therefore, C3(H2O) generation in vivo may be less important for AP activation during specific attack or dysregulated homeostasis, but may be an important ligand for C3 receptors in cell-cell interactions and a source of C3 for the intracellular complement reservoir.

  • 25.
    Nilsson, Per H.
    et al.
    University of Oslo, Rikshospitalet, Norway.
    Berg, A.
    e, Stavanger University Hospital, Norway ; Hospital of Maputo, Mozambique ; University of Bergen, Norway.
    Otterdal, K.
    University of Oslo, Rikshospitalet, Norway.
    Patel, S.
    Hospital of Maputo, Mozambique.
    Gonca, M.
    Hospital of Maputo, Mozambique.
    David, C.
    Hospital of Maputo, Mozambique.
    Dalen, I.
    Stavanger University Hospital, , Norway.
    Nymo, S.
    University of Oslo, Rikshospitalet, Norway ; Research Laboratory Nordland Hospital, Norway ; University of Tromsø, Norway.
    Nilsson, M.
    University of Oslo, Rikshospitalet, Norway.
    Ueland, T.
    University of Oslo, Rikshospitalet, Norway ; University of Oslo, Norway.
    Prato, M.
    University of Torino Medical School, Italy.
    Giribaldi, G.
    University of Torino Medical School, Italy.
    Aukrust, P.
    University of Oslo, Rikshospitalet, Norway.
    Langeland, N.
    University of Bergen, Norway.
    Mollnes, T. E.
    University of Oslo, Rikshospitalet, Norway.
    Complement-dependent inflammatory response Plasmodium-derived hemozoin in malaria2014Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 61, nr 2, s. 230-230Artikel i tidskrift (Refereegranskat)
  • 26.
    Nilsson, Per H.
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Univ Oslo, Norway.
    Johnson, Christina
    Oslo Univ Hosp, Norway;Univ Oslo, Norway.
    Pischke, Soren E.
    Oslo Univ Hosp, Norway;Univ Oslo, Norway.
    Fure, Hilde
    Nordland Hosp, Norway;Univ Tromso, Norway.
    Landsem, Anne
    Nordland Hosp, Norway;Univ Tromso, Norway.
    Bergseth, Grethe
    Nordland Hosp, Norway;Univ Tromso, Norway.
    Haugaard-Kedström, Linda M.
    Univ Copenhagen, Denmark.
    Huber-Lang, Markus
    Univ Hosp Ulm, Germany.
    Brekke, Ole-Lars
    Nordland Hosp, Norway;Univ Tromso, Norway.
    Mollnes, Tom Eirik
    Oslo Univ Hosp, Norway;Univ Oslo, Norway;Nordland Hosp, Norway;Univ Tromso, Norway;Norwegian Univ Sci & Technol, Norway.
    Characterization of a novel whole blood model for the study of thrombin in complement activation and inflammation2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 136-137Artikel i tidskrift (Övrigt vetenskapligt)
  • 27.
    Nilsson, Per H.
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). University of Oslo, Rikshospitalet.
    Johnson, Christina
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Pischke, Søren E
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Fure, Hilde
    Nordland Hospital, Norway;University of Tromsø, Norway.
    Landsem, Anne
    Nordland Hospital, Norway;University of Tromsø, Norway.
    Bergseth, Grethe
    Nordland Hospital, Norway;University of Tromsø, Norway.
    Haugaard-Kedström, Linda M.
    University of Copenhagen, Denmark.
    Huber-Lang, Markus
    University Hospital of Ulm, Germany.
    Brekke, Ole-Lars
    Nordland Hospital, Norway;University of Tromsø, Norway.
    Mollnes, Tom Eirik
    Oslo University Hospital, Norway;University of Oslo, Norway;Nordland Hospital, Norway;University of Tromsø, Norway.
    Characterization of a novel whole blood model for the study of thrombin in complement activation and inflammation2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, nr SI: EMCHD2017, s. 136-137Artikel i tidskrift (Refereegranskat)
  • 28.
    Nilsson, Per H.
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Oslo Univ Hosp, Norway;Univ Oslo, Norway.
    Thomas, Anub Mathew
    Oslo Univ Hosp, Norway.
    Bergseth, Grethe
    Nordland Hosp, Norway.
    Gustavsen, Alice
    Oslo Univ Hosp, Norway.
    Volokhina, Elena B.
    Radboud Univ Nijmegen, Netherlands;Radboud Univ Nijmegen, Netherlands.
    van den Heuvel, Lambertus P.
    Radboud Univ Nijmegen, Netherlands;Univ Hosp Leuven, Belgium.
    Barratt-Due, Andreas
    Oslo Univ Hosp, Norway.
    Mollnes, Tom E.
    Oslo Univ Hosp, Rikshosp, Norway;Univ Oslo, Norway;Nordland Hosp, Norway;Univ Tromso, Norway;Norwegian Univ Sci & Technol, Norway.
    Eculizumab-C5 complexes express a C5a neoepitope in vivo: Consequences for interpretation of patient complement analyses2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 111-114Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The complement system has obtained renewed clinical focus due to increasing number of patients treated with eculizumab, a monoclonal antibody inhibiting cleavage of C5 into C5a and C5b. The FDA approved indications are paroxysmal nocturnal haemoglobinuria and atypical haemolytic uremic syndrome, but many other diseases are candidates for complement inhibition. It has been postulated that eculizumab does not inhibit C5a formation in vivo, in contrast to what would be expected since it blocks C5 cleavage. We recently revealed that this finding was due to a false positive reaction in a C5a assay. In the present study, we identified expression of a neoepitope which was exposed on C5 after binding to eculizumab in vivo. By size exclusion chromatography of patient serum obtained before and after infusion of eculizumab, we document that the neoepitope was exposed in the fractions containing the eculizumab-C5 complexes, being positive in this actual C5a assay and negative in others. Furthermore, we confirmed that it was the eculizumab-C5 complexes that were detected in the C5a assay by adding an anti-IgG4 antibody as detection antibody. Competitive inhibition by anti-C5 antibodies localized the epitope to the C5a moiety of C5. Finally, acidification of C5, known to alter C5 conformation, induced a neoepitope reacting identical to the one we explored, in the C5a assays. These data are important for interpretation of complement analyses in patients treated with eculizumab.

  • 29.
    Orrem, Hilde L
    et al.
    Oslo University Hospital, Rikshospitalet, Norway.
    Nilsson, Per H.
    Oslo University Hospital, Rikshospitalet, Norway.
    Pischke, Søren E
    Oslo University Hospital, Rikshospitalet, Norway.
    Kleveland, Ola
    St. Olavs Hospital, Trondheim, Norway.
    Ekholt, Karin
    Oslo University Hospital, Rikshospitalet, Norway.
    Aukrust, Pål
    Oslo University Hospital, Norway.
    Halvorsen, Bente
    Oslo University Hospital, Norway.
    Gullestad, Lars
    University of Oslo, Norway.
    Barratt-Due, Andreas
    Oslo University Hospital, Rikshospitalet, Norway.
    Mollnes, Tom E
    Oslo University Hospital, Rikshospitalet, Norway.
    The IL-6 receptor inhibitor tocilizumab attenuated expression of C5a receptor 1 and 2 in patients with myocardial infarction2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, s. 128-128Artikel i tidskrift (Refereegranskat)
  • 30.
    Ricklin, Daniel
    et al.
    Univ Penn, USA.
    Sfyroera, Georgia
    Univ Penn, USA.
    Reis, Edimara
    Univ Penn, USA.
    Chen, Hui
    Univ Penn, USA.
    Wu, Emilia
    Univ Minnesota, USA.
    Kaznessis, Yiannis
    Univ Minnesota, USA.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Lambris, John D.
    Univ Penn, USA.
    Rare loss-of-function mutation in C3 provides insight into molecular and pathophysiological determinants of alternative pathway activity2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 174-174Artikel i tidskrift (Övrigt vetenskapligt)
  • 31.
    Sandholm, Kerstin
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Wijkstrom, Elisabeth
    University Hospital, Uppsala.
    Skattum, Lillemor
    Lund University.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Validations of assays for the evaluation of C1q in inflammatory diseases and thromboinflammation2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 176-177Artikel i tidskrift (Övrigt vetenskapligt)
  • 32.
    Shahini, Negar
    et al.
    Oslo University Hospital, Rikshospitalet, Norway.
    Michelsen, Annika E
    University of Oslo, Norway.
    Nilsson, Per H.
    University of Oslo, Norway.
    Ekholt, Karin
    University of Oslo, Norway.
    Gullestad, Lars
    Oslo University Hospital, Rikshospitalet, Norway.
    Broch, Kaspar
    Oslo University Hospital, Rikshospitalet, Norway.
    Dahl, Christen P
    Oslo University Hospital, Rikshospitalet, Norway.
    Aukrust, Pål
    Oslo University Hospital, Rikshospitalet, Norway.
    Ueland, Thor
    Oslo University Hospital, Rikshospitalet, Norway.
    Mollnes, Tom Eirik
    Oslo University Hospital, Rikshospitalet, Norway.
    Yndestad, Arne
    Oslo University Hospital, Rikshospitalet, Norway.
    Louwe, Mieke C
    Oslo University Hospital, Rikshospitalet, Norway.
    The alternative complement pathway is dysregulated in patients with chronic heart failure2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, nr SI: EMCHD2017, s. 127-127Artikel i tidskrift (Refereegranskat)
  • 33.
    Speth, Cornelia
    et al.
    Med Univ Innsbruck, Austria.
    Rambach, Guenter
    Med Univ Innsbruck, Austria.
    Wuerzner, Reinhard
    Med Univ Innsbruck, Austria.
    Lass-Floerl, Cornelia
    Med Univ Innsbruck, Austria.
    Kozarcanin, Huda
    Uppsala University.
    Hamad, Osama A.
    Uppsala University.
    Nilsson, Bo
    Uppsala University.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement and platelets: Mutual interference in the immune network2015Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, nr 1, s. 108-118Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    In recent years, the view of platelets has changed from mere elements of hemostasis to immunological multitaskers. They are connected in manifold ways to other cellular and humoral components of the immune network, one of which is the complement system, a potent player in soluble innate immunity. Our article reviews the crucial and complex interplay between platelets and complement, focusing on mutual regulation of these two interaction partners by their respective molecular mechanisms. Furthermore, the putative relevance of these processes to infectious diseases, inflammatory conditions, and autoimmune disorders, as well as the treatment of patients with biomaterials is highlighted. (C) 2015 Elsevier Ltd. All rights reserved.

  • 34.
    Thomas, Anub Mathew
    et al.
    Oslo Univ Hosp, Norway;Univ Oslo, Norway.
    Gerogianni, Alexandra
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Barratt-Due, Andreas
    Oslo Univ Hosp, Norway;Univ Oslo, Norway.
    McAdam, Martin B.
    Oslo Univ Hosp, Norway;Univ Oslo, Norway.
    Mollnes, Tom Eirik
    Oslo Univ Hosp, Norway;Univ Oslo, Norway;Nordland Hosp, Norway;Univ Tromso, Norway;Norwegian Univ Sci & Technol, Norway.
    Nilsson, Per H.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Oslo Univ Hosp, Norway;Univ Oslo, Norway.
    Complement (C5)-inhibition attenuates heme-induced inflammation in human whole blood2018Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 102, s. 220-220Artikel i tidskrift (Övrigt vetenskapligt)
  • 35.
    Thomas, Anub Mathew
    et al.
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Schjalm, Camilla
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Nilsson, Per H.
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Lindenskov, Paal H H
    Oslo University Hospital, Norway.
    Rørtveit, Runa
    Norwegian University of Life Sciences Oslo/Ås, Norway.
    Solberg, Rønnaug
    Oslo University Hospital, Norway.
    Saugstad, Ola Didrik
    Oslo University Hospital, Norway.
    Berglund, Magnus M
    Swedish Orphan Biovitrum.
    Strömberg, Patrik
    Swedish Orphan Biovitrum.
    Jansen, Johan Høgset
    Norwegian University of Life Sciences Oslo/Ås, Norway.
    Castellheim, Albert
    Queen Silvia Children's Hospital.
    Mollnes, Tom Eirik
    Oslo University Hospital, Norway;Nordland Hospital, Norway;University of Tromsø, Norway.
    Barratt-Due, Andreas
    Oslo University Hospital, Norway;University of Oslo, Norway.
    Combined inhibition of C5 and CD14 attenuates systemic inflammation in a newborn pig-model of meconium aspiration syndrome2017Ingår i: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 89, nr SI: EMCHD2017, s. 166-167Artikel i tidskrift (Refereegranskat)
1 - 35 av 35
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