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  • 1.
    Aksel Jacobsen, Freja
    et al.
    Novo Nordisk A/S, Bagsværd, Denmark.
    Andersson, Åsa
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS).
    Inhibitors of intracellular enzymes for treatment of multiple sclerosis2019In: Atlas of ScienceArticle, review/survey (Other (popular science, discussion, etc.))
  • 2.
    Aksel Jacobsen, Freja
    et al.
    University of Copenhagen, Copenhagen, Denmark & Novo Nordisk A/S, Bagsværd, Denmark.
    Scherer, Alexander N.
    Yale University School of Medicine, New Haven, CT, USA.
    Mouritsen, Jeppe
    University of Copenhagen, Copenhagen, Denmark & Novozymes A/S, Bagsværd, Denmark.
    Bragadóttir, Hera
    University of Copenhagen, Copenhagen, Denmark & Xelia Pharmaceuticals A/S, Copenhagen, Denmark.
    Bäckström, B. Thomas
    Novo Nordisk A/S, Måløv, Denmark & BTB Pharma, Malmö, Sweden.
    Sardar, Samra
    University of Copenhagen, Copenhagen, Denmark.
    Holmberg, Dan
    Lund University, Malmö, Sweden.
    Koleske, Anthony J.
    Yale University School of Medicine, New Haven, CT, USA.
    Andersson, Åsa
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). University of Copenhagen, Copenhagen, Denmark.
    A Role for the Non-Receptor Tyrosine Kinase Abl2/Arg in Experimental Neuroinflammation2018In: Journal of Neuroimmune Pharmacology, ISSN 1557-1890, E-ISSN 1557-1904, Vol. 13, no 2, p. 265-276Article in journal (Refereed)
    Abstract [en]

    Multiple sclerosis is a neuroinflammatory degenerative disease, caused by activated immune cells infiltrating the CNS. The disease etiology involves both genetic and environmental factors. The mouse genetic locus, Eae27, linked to disease development in the experimental autoimmune encephalomyelitis (EAE) model for multiple sclerosis, was studied in order to identify contributing disease susceptibility factors and potential drug targets for multiple sclerosis. Studies of an Eae27 congenic mouse strain, revealed that genetic variation within Eae27 influences EAE development. The Abl2 gene, encoding the non-receptor tyrosine kinase Arg, is located in the 4,1 megabase pair long Eae27 region. The Arg protein plays an important role in cellular regulation and is, in addition, involved in signaling through the B- and T-cell receptors, important for the autoimmune response. The presence of a single nucleotide polymorphism causing an amino acid change in a near actin-interacting domain of Arg, in addition to altered lymphocyte activation in the congenic mice upon immunization with myelin antigen, makes Abl2/Arg a candidate gene for EAE. Here we demonstrate that the non-synonymous SNP does not change Arg’s binding affinity for F-actin but suggest a role for Abl kinases in CNS inflammation pathogenesis by showing that pharmacological inhibition of Abl kinases ameliorates EAE, but not experimental arthritis. © 2018 The Author(s)

  • 3.
    Andersson, Åsa
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). Köpenhamns universitet, Köpenhamn, Danmark.
    Abl-tyrosinkinaser och multipel skleros2018In: BestPractice, Vol. 6, no 24, p. 14-16Article, review/survey (Other academic)
  • 4.
    Andersson, Åsa
    et al.
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). University of Copenhagen, Copenhagen, Denmark.
    Aksel Jacobsen, Freja
    Copenhagen University, Copenhagen, Denmark.
    B-cells and Inflammation in the Absence of the Abelson Related Gene (Arg)2016In: Journal of Clinical & Cellular Immunology, ISSN 2155-9899, E-ISSN 2155-9899, Vol. 7, no 6, article id 1000470Article in journal (Refereed)
    Abstract [en]

    The Abelson non-receptor tyrosine kinases, c-Abl and Arg, are important regulators of cellular processes in cancer, inflammation, infection, and neuronal dynamics. Recent research on the role for these kinases in processes involving interactions with the cytoskeleton or signaling molecules, may lead to further insight into the pathogenesis of a variety of disorders, including chronic inflammatory diseases. In a mouse model for multiple sclerosis, we recently reported that Arg deficient mice develop T-cell mediated autoimmune neuro-inflammation with the same severity as littermate controls, but display a different B-cell phenotype upon immunization. Here we comment on these results and discuss the role for Arg in B-cell activation and homeostasis.

  • 5.
    Andersson, Åsa
    et al.
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). Department of Drug Design and Pharmacology, Copenhagen University, Copenhagen, Denmark.
    Sardar, Samra
    Nordic Bioscience, Copenhagen, Denmark.
    A transcriptional regulator controlling severity in experimental arthritis2019In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 78, no Suppl. 2, p. 667-667, article id FRI0011Article in journal (Refereed)
    Abstract [en]

    Background: Susceptibility to Rheumatoid Arthritis (RA) is dependent on complex interactions among genetic and environmental factors. Protein candidates and their role in pathways leading to chronic inflammation of the joints, in addition to their potential as drug targets, can be revealed with the help of experimental models for disease (1). From the results of functional genetic studies, we have recently shown that the T-box gene, TBX3, is a candidate gene in Collagen Induced Arthritis (CIA), an experimental model for RA (2). TBX3 encodes a transcriptional regulator involved in differentiation of several organs, including bone, during embryonic development. It has, in addition, been demonstrated important in oncogenesis (3). Our studies suggest that TBX3 has a role in B-cell activation and is important for the severity of disease in the CIA model (2). Objectives: The objective of this project is to understand the role for the transcriptional regulator TBX3 in development of RA. Methods: Bioinformatics based comparative studies of mouse and human alleles in the regulatory region of TBX3. CRISPR/Cas9-introduced deletions and base modifications in human B-cell lines. Activation of genetically modified B-cells in vitro, followed by analyses of proliferative response and antibody production. Results: Studies of CIA development in mice with single nucleotide polymorphisms (SNPs) in the regulatory region of Tbx3 revealed a significant difference in severity of arthritis. In line with this, the anti-collagen type II antibody titers were shown substantially higher in mice with more severe arthritis, even before onset of disease. In addition, preliminary data shows that the proliferative response to Type II collagen upon re-challenge of lymph node cells in vitro is higher in these mice, suggesting a more active response to the disease-inducing antigen. Because the TBX3 gene is conserved between mouse and human, we are investigating whether similar genetic variations are found in the regulatory region of the human TBX3 gene and whether the putative genetic variation would lead to a distinct B-cell phenotype upon activation in vitro. Conclusion: We suggest that the oncoprotein TBX3 is a novel candidate contributing to disease severity in experimental arthritis. Investigations of genetic variation in the TBX3 gene and its role in the activation of human B-cells will reveal whether this protein is a candidate for influencing also development of RA.

  • 6.
    Jacobsen, Freja A.
    et al.
    Dept. of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark & Novo Nordisk A/S, Gentofte, Denmark.
    Hulst, Camilla
    Dept. of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark & Novo Nordisk A/S, Gentofte, Denmark.
    Bäckström, Thomas
    Novo Nordisk A/S, Måløv, Denmark & BTB Pharma, Malmö, Sweden.
    Koleske, Anthony J.
    Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, USA.
    Andersson, Åsa
    Dept. of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark.
    Arg Deficiency Does not Influence the Course of Myelin Oligodendrocyte Glycoprotein (MOG35-55)-induced Experimental Autoimmune Encephalomyelitis2016In: Journal of Clinical & Cellular Immunology, ISSN 2155-9899, E-ISSN 2155-9899, Vol. 7, no 3, article id 1000420Article in journal (Refereed)
    Abstract [en]

    Background: Inhibition of Abl kinases has an ameliorating effect on the rodent model for multiple sclerosis, experimental autoimmune encephalomyelitis, and arrests lymphocyte activation. The family of Abl kinases consists of the Abl1/Abl and Abl2/Arg tyrosine kinases. While the Abl kinase has been extensively studied in immune activation, roles for Arg are incompletely characterized. To investigate the role for Arg in experimental autoimmune encephalomyelitis, we studied disease development in Arg-/- mice.

    Methods: Arg-/- and Arg+/+ mice were generated from breeding of Arg+/- mice on the C57BL/6 background. Mice were immunized with the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide and disease development recorded. Lymphocyte phenotypes of wild type Arg+/+ and Arg-/- mice were studied by in vitro stimulation assays and flow cytometry.

    Results: The breeding of Arg+/+ and Arg-/- mice showed skewing in the frequency of born Arg-/- mice. Loss of Arg function did not affect development of experimental autoimmune encephalomyelitis, but reduced the number of splenic B-cells in Arg-/- mice following immunization with MOG peptide.

    Conclusions: Development of MOG-induced experimental autoimmune encephalomyelitis is not dependent on Arg, but Arg plays a role for the number of B cells in immunized mice. This might suggest a novel role for the Arg kinase in B-cell trafficking or regulation. Furthermore, the results suggest that Arg is important for normal embryonic development. © 2016 Jacobsen FA, et al.

  • 7.
    Nygren, Jens Martin
    et al.
    Hematopoietic Stem Cell Laboratory, Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University, Lund, Sweden.
    Bryder, David
    Hematopoietic Stem Cell Laboratory, Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University, Lund, Sweden.
    Jacobsen, Sten Eirik W
    Hematopoietic Stem Cell Laboratory, Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University, Lund, Sweden.
    Prolonged cell cycle transit is a defining and developmentally conserved hemopoietic stem cell property2006In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 177, no 1, p. 201-208Article in journal (Refereed)
    Abstract [en]

    Adult mouse hemopoietic stem cells (HSCs) are typically quiescent and enter and progress through the cell cycle rarely in steady-state bone marrow, but their rate of proliferation can be dramatically enhanced on demand. We have studied the cell cycle kinetics of HSCs in the developing fetal liver at a stage when they expand extensively. Despite that 100% of fetal liver HSCs divide within a 48-h period, their average cell cycle transit time (10.6 h) is twice that of their downstream progenitors, translating into a prolonged G(1) transit and a period of relative quiescence (G(0)). In agreement with their prolonged G(1) transit when compared with hemopoietic progenitors, competitive transplantation experiments demonstrate that fetal HSCs are highly enriched in G(1) but also functional in S-G(2)-M. This observation combined with experimental data demonstrating that adult HSCs forced to expand ex vivo also sustain a uniquely prolonged cell cycle and G(1) transit, demonstrate at least in part why purified HSCs at any state of development or condition are highly enriched in the G(0)-G(1) phases of the cell cycle. We propose that a uniquely prolonged cell cycle transit is a defining stem cell property, likely to be critical for their maintenance and self-renewal throughout development.

  • 8.
    Sardar, Samra
    et al.
    University of Copenhagen, Copenhagen, Denmark.
    Alish, Kerr
    University of Copenhagen, Copenhagen, Denmark & Pfizer Pharmaceuticals, Dublin, Ireland.
    Vaartjes, Daniëlle
    University of Copenhagen, Copenhagen, Denmark & Karolinska Institute, Stockholm, Sweden.
    Voetmann, Mathilde Emilie
    University of Copenhagen, Copenhagen, Denmark & Biogen Denmark A/S, Hillerød, Denmark.
    Moltved, Emilie Riis
    University of Copenhagen, Copenhagen, Denmark & QuintilesIMS, North Carolina, USA.
    Andersson, Åsa
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). University of Copenhagen, Copenhagen, Denmark.
    A novel candidate for genetic control of Collagen Induced Arthritis is involved in transcriptional regulation of B-cell proliferation2017Conference paper (Other academic)
  • 9.
    Sardar, Samra
    et al.
    University of Copenhagen, Copenhagen, Denmark & Nordic Bioscience A/S, Copenhagen, Denmark.
    Kanne, Katrine
    University of Copenhagen, Copenhagen, Denmark & Novartis International AG, Copenhagen, Denmark.
    Andersson, Åsa
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). University of Copenhagen, Copenhagen, Denmark.
    Analysis of polymorphisms in the mediator complex subunit 13-like (Med13L) gene in the context of immune function and development of experimental arthritis2018In: Archivum Immunologiae et Therapiae Experimentalis, ISSN 0004-069X, E-ISSN 1661-4917, Vol. 66, no 5, p. 365-377Article in journal (Refereed)
    Abstract [en]

    The Mediator complex subunit 13-like (MED13L) protein is part of the multi-protein mediator complex and plays an important role in gene transcription. Polymorphisms in the MED13L gene have been linked to congenital heart anomalies and intellectual disabilities. Despite recent evidence of indirect links of MED13L to cytokine release and inflammation, impact of genetic variations in MED13L on immune cells remains unexplored. The B10.RIII and RIIIS/J mouse strains vary in susceptibility to induced experimental autoimmune disease models. From sequencing data of the two mouse strains, we identified six polymorphisms in the coding regions of Med13l. By using congenic mice, we studied the effect of these polymorphisms on immune cell development and function along with susceptibility to collagen-induced arthritis, an animal model for Rheumatoid Arthritis (RA). Combining in vivo disease data, in vitro functional data, and computational analysis of the reported non-synonymous polymorphisms, we report that genetic polymorphisms in Med13l do not affect the immune phenotype in these mice and are predicted to be non-disease associated. © The Author(s) 2018

  • 10.
    Sardar, Samra
    et al.
    Nordic Bioscience A/S, Copenhagen, Denmark.
    Kerr, Alish
    Nuritas, Dublin, Ireland.
    Vaartjes, Daniëlle
    Karolinska Institutet, Stockholm, Sweden.
    Moltved, Emilie Riis
    IQVIA Denmark, Copenhagen, Denmark.
    Karosiene, Edita
    Novo Nordisk A/S, Copenhagen, Denmark.
    Gupta, Ramneek
    Technical University of Denmark, Lyngby, Denmark.
    Andersson, Åsa
    Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS).
    The oncoprotein TBX3 is controlling severity in experimental arthritis2019In: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 21, no 1, article id 16Article in journal (Refereed)
    Abstract [en]

    Background: Development of autoimmune diseases is the result of a complex interplay between hereditary and environmental factors, with multiple genes contributing to the pathogenesis in human disease as well as in experimental models for disease. The T-box protein 3 is a transcriptional repressor essential during early embryonic development, in the formation of bone and additional organ systems, and in tumorigenesis.

    Methods: With the aim to find novel genes important for autoimmune inflammation, we have performed genetic studies of collagen-induced arthritis, a mouse experimental model for Rheumatoid Arthritis.

    Results: We show that a small genetic fragment on mouse chromosome 5, including Tbx3 and three additional protein-coding genes, is linked to severe arthritis and high titers of anti-collagen antibodies. Gene expression studies have revealed differential expression of Tbx3 in B-cells, where low expression was accompanied by a higher B-cell response upon B-cell receptor stimulation in vitro. Furthermore, we show that serum TBX3 levels rise concomitantly with increasing severity of CIA.

    Conclusions: From these results, we suggest that TBX3 is a novel factor important for the regulation of gene transcription in the immune system and that genetic polymorphisms, resulting in lower expression of Tbx3, are contributing to a more severe form of collagen-induced arthritis and high titers of autoantibodies. We also propose TBX3 as a putative diagnostic biomarker for rheumatoid arthritis.

  • 11.
    Sardar, Samra
    et al.
    University of Copenhagen, Copenhagen, Denmark.
    Vartjes, Daniëlle
    Karolinska Institute, Stockholm, Sweden.
    Voetmann, Mathilde
    University of Copenhagen.
    Andersson, Åsa
    University of Copenhagen, Copenhagen, Denmark.
    Novel candidates for genetic control of Collagen INduced Arthritis are involved in transcriptional regulation of B-cell proliferation2017Conference paper (Refereed)
  • 12.
    Thorén, Lina A.
    et al.
    Lunds Universitet, Lund, Sverige.
    Liuba, Karina
    Lunds Universitet, Lund, Sverige.
    Bryder, David
    Lunds Universitet, Lund, Sverige.
    Nygren, Jens Martin
    Lunds universitet, Lund, Sverige.
    Jensen, Christina T
    Lunds Universitet, Lund, Sverige.
    Qian, Hong
    Lunds Universitet, Lund, Sverige.
    Antonchuk, Jennifer
    Lunds Universitet, Lund, Sverige.
    Jacobsen, Sten-Eirik W
    Lunds Universitet, Lund, Sverige.
    Kit regulates maintenance of quiescent hematopoietic stem cells2008In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 180, no 4, p. 2045-2053Article in journal (Refereed)
    Abstract [en]

    Hematopoietic stem cell (HSC) numbers are tightly regulated and maintained in postnatal hematopoiesis. Extensive studies have supported a role of the cytokine tyrosine kinase receptor Kit in sustaining cycling HSCs when competing with wild-type HSCs posttransplantation, but not in maintenance of quiescent HSCs in steady state adult bone marrow. In this study, we investigated HSC regulation in White Spotting 41 (Kit(W41/W41)) mice, with a partial loss of function of Kit. Although the extensive fetal HSC expansion was Kit-independent, adult Kit(W41/W41) mice had an almost 2-fold reduction in long-term HSCs, reflecting a loss of roughly 10,000 Lin(-)Sca-1(+)Kit(high) (LSK)CD34(-)Flt3(-) long-term HSCs by 12 wk of age, whereas LSKCD34(+)Flt3(-) short-term HSCs and LSKCD34(+)Flt3(+) multipotent progenitors were less affected. Whereas homing and initial reconstitution of Kit(W41/W41) bone marrow cells in myeloablated recipients were close to normal, self-renewing Kit(W41/W41) HSCs were progressively depleted in not only competitive but also noncompetitive transplantation assays. Overexpression of the anti-apoptotic regulator BCL-2 partially rescued the posttransplantation Kit(W41/W41) HSC deficiency, suggesting that Kit might at least in the posttransplantation setting in part sustain HSC numbers by promoting HSC survival. Most notably, accelerated in vivo BrdU incorporation and cell cycle kinetics implicated a previously unrecognized role of Kit in maintaining quiescent HSCs in steady state adult hematopoiesis.

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