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  • 1.
    Bruhn, Sören
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Fang, Yu
    Guiyang Medical Coll, Peoples R China University of Gothenburg, Sweden .
    Barrenäs, Fredrik
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Gustafsson, Mika
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Zhang, Huan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Konstantinell, Aelita
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Kronke, Andrea
    Cenix BioScience GmbH, Germany .
    Sonnichsen, Birte
    Cenix BioScience GmbH, Germany .
    Bresnick, Anne
    Albert Einstein Coll Med, NY 10461 USA .
    Dulyaninova, Natalya
    Albert Einstein Coll Med, NY 10461 USA .
    Wang, Hui
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Zhao, Yelin
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Klingelhofer, Jorg
    University of Copenhagen, Denmark .
    Ambartsumian, Noona
    University of Copenhagen, Denmark .
    Beck, Mette K.
    Technical University of Denmark, Denmark .
    Nestor, Colm
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Bona, Elsa
    Boras Hospital, Sweden .
    Xiang, Zou
    University of Gothenburg, Sweden .
    Benson, Mikael
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Allergy Center. Östergötlands Läns Landsting, Center of Paediatrics and Gynaecology and Obstetrics, Department of Paediatrics in Linköping.
    A Generally Applicable Translational Strategy Identifies S100A4 as a Candidate Gene in Allergy2014In: Science Translational Medicine, ISSN 1946-6234, E-ISSN 1946-6242, Vol. 6, no 218Article in journal (Refereed)
    Abstract [en]

    The identification of diagnostic markers and therapeutic candidate genes in common diseases is complicated by the involvement of thousands of genes. We hypothesized that genes co-regulated with a key gene in allergy, IL13, would form a module that could help to identify candidate genes. We identified a T helper 2 (T(H)2) cell module by small interfering RNA-mediated knockdown of 25 putative IL13-regulating transcription factors followed by expression profiling. The module contained candidate genes whose diagnostic potential was supported by clinical studies. Functional studies of human TH2 cells as well as mouse models of allergy showed that deletion of one of the genes, S100A4, resulted in decreased signs of allergy including TH2 cell activation, humoral immunity, and infiltration of effector cells. Specifically, dendritic cells required S100A4 for activating T cells. Treatment with an anti-S100A4 antibody resulted in decreased signs of allergy in the mouse model as well as in allergen-challenged T cells from allergic patients. This strategy, which may be generally applicable to complex diseases, identified and validated an important diagnostic and therapeutic candidate gene in allergy.

  • 2.
    Cao, Yihai
    et al.
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences.
    Arbiser, Jack
    Emory University.
    DAmato, Robert J
    Childrens Hospital, Boston.
    DAmore, Patricia A
    Harvard University.
    Ingber, Donald E
    Childrens Hospital, Boston.
    Kerbel, Robert
    Sunnybrook Health Science Centre.
    Klagsbrun, Michael
    Childrens Hospital, Boston.
    Lim, Sharon
    Karolinska Institute.
    Moses, Marsha A
    Childrens Hospital, Boston.
    Zetter, Bruce
    Childrens Hospital, Boston.
    Dvorak, Harold
    Harvard University.
    Langer, Robert
    MIT.
    Forty-Year Journey of Angiogenesis Translational Research2011In: Science Translational Medicine, ISSN 1946-6234, E-ISSN 1946-6242, Vol. 3, no 114Article, review/survey (Refereed)
    Abstract [en]

    Forty years ago, Judah Folkman predicted that tumor growth is dependent on angiogenesis and that inhibiting this process might be a new strategy for cancer therapy. This hypothesis formed the foundation of a new field of research that represents an excellent example of how a groundbreaking scientific discovery can be translated to yield benefits for patients. Today, antiangiogenic drugs are used to treat human cancers and retinal vascular diseases. Here, we guide readers through 40 years of angiogenesis research and discuss challenges of antiangiogenic therapy.

  • 3.
    Gustafsson, Mika
    et al.
    Linköping University, Department of Physics, Chemistry and Biology, Bioinformatics. Linköping University, Faculty of Science & Engineering.
    Gawel, Danuta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Alfredsson, Lars
    Karolinska Institute, Sweden.
    Baranzini, Sergio
    University of Calif San Francisco, CA, USA.
    Bjorkander, Janne
    County Council Jonköping, Sweden.
    Blomgran, Robert
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Hellberg, Sandra
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Eklund, Daniel
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Ernerudh, Jan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Immunology and Transfusion Medicine.
    Kockum, Ingrid
    Karolinska Institute, Sweden; Centre Molecular Med, Sweden.
    Konstantinell, Aelita
    Linköping University, Faculty of Medicine and Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Arctic University of Norway, Norway.
    Lahesmaa, Riita
    University of Turku, Finland; Abo Akad University, Finland.
    Lentini, Antonio
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Liljenström, H. Robert I.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Mattson, Lina
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Matussek, Andreas
    County Council Jonköping, Sweden.
    Mellergård, Johan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Local Health Care Services in Central Östergötland, Department of Neurology.
    Mendez, Melissa
    University of Peruana Cayetano Heredia, Peru.
    Olsson, Tomas
    Karolinska Institute, Sweden; Centre Molecular Med, Sweden.
    Pujana, Miguel A.
    Catalan Institute Oncol, Spain.
    Rasool, Omid
    University of Turku, Finland; Abo Akad University, Finland.
    Serra-Musach, Jordi
    Catalan Institute Oncol, Spain.
    Stenmarker, Margaretha
    County Council Jonköping, Sweden.
    Tripathi, Subhash
    University of Turku, Finland; Abo Akad University, Finland.
    Viitala, Miro
    University of Turku, Finland; Abo Akad University, Finland.
    Wang, Hui
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. University of Texas MD Anderson Cancer Centre, TX 77030 USA.
    Zhang, Huan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Nestor, Colm
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Benson, Mikael
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    A validated gene regulatory network and GWAS identifies early regulators of T cell-associated diseases2015In: Science Translational Medicine, ISSN 1946-6234, E-ISSN 1946-6242, Vol. 7, no 313, article id 313ra178Article in journal (Refereed)
    Abstract [en]

    Early regulators of disease may increase understanding of disease mechanisms and serve as markers for presymptomatic diagnosis and treatment. However, early regulators are difficult to identify because patients generally present after they are symptomatic. We hypothesized that early regulators of T cell-associated diseases could be found by identifying upstream transcription factors (TFs) in T cell differentiation and by prioritizing hub TFs that were enriched for disease-associated polymorphisms. A gene regulatory network (GRN) was constructed by time series profiling of the transcriptomes and methylomes of human CD4(+) T cells during in vitro differentiation into four helper T cell lineages, in combination with sequence-based TF binding predictions. The TFs GATA3, MAF, and MYB were identified as early regulators and validated by ChIP-seq (chromatin immunoprecipitation sequencing) and small interfering RNA knockdowns. Differential mRNA expression of the TFs and their targets in T cell-associated diseases supports their clinical relevance. To directly test if the TFs were altered early in disease, T cells from patients with two T cell-mediated diseases, multiple sclerosis and seasonal allergic rhinitis, were analyzed. Strikingly, the TFs were differentially expressed during asymptomatic stages of both diseases, whereas their targets showed altered expression during symptomatic stages. This analytical strategy to identify early regulators of disease by combining GRNs with genome-wide association studies may be generally applicable for functional and clinical studies of early disease development.

  • 4.
    Herrmann, Uli S.
    et al.
    University of Zurich Hospital, Switzerland.
    Schuetz, Anne K.
    ETH, Switzerland.
    Shirani, Hamid
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering.
    Huang, Danzhi
    University of Zurich, Switzerland.
    Saban, Dino
    University of Zurich Hospital, Switzerland.
    Nuvolone, Mario
    University of Zurich Hospital, Switzerland.
    Li, Bei
    University of Zurich Hospital, Switzerland.
    Ballmer, Boris
    University of Zurich Hospital, Switzerland.
    Åslund, Andreas
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, The Institute of Technology.
    Mason, Jeffrey
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, The Institute of Technology.
    Rushing, Elisabeth
    University of Zurich Hospital, Switzerland.
    Budka, Herbert
    University of Zurich Hospital, Switzerland.
    Nyström, Sofie
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering.
    Hammarström, Per
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering.
    Boeckmann, Anja
    University of Lyon 1, France.
    Caflisch, Amedeo
    University of Zurich, Switzerland.
    Meier, Beat H.
    ETH, Switzerland.
    Nilsson, Peter
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering.
    Hornemann, Simone
    University of Zurich Hospital, Switzerland.
    Aguzzi, Adriano
    University of Zurich Hospital, Switzerland.
    Structure-based drug design identifies polythiophenes as antiprion compounds2015In: Science Translational Medicine, ISSN 1946-6234, E-ISSN 1946-6242, Vol. 7, no 299, p. 299ra123-Article in journal (Refereed)
    Abstract [en]

    Prions cause transmissible spongiform encephalopathies for which no treatment exists. Prions consist of PrPSc, a misfolded and aggregated form of the cellular prion protein (PrPC). We explore the antiprion properties of luminescent conjugated polythiophenes (LCPs) that bind and stabilize ordered protein aggregates. By administering a library of structurally diverse LCPs to the brains of prion-infected mice via osmotic minipumps, we found that antiprion activity required a minimum of five thiophene rings bearing regularly spaced carboxyl side groups. Solid-state nuclear magnetic resonance analyses and molecular dynamics simulations revealed that anionic side chains interacted with complementary, regularly spaced cationic amyloid residues of model prions. These findings allowed us to extract structural rules governing the interaction between LCPs and protein aggregates, which we then used to design a new set of LCPs with optimized binding. The new set of LCPs showed robust prophylactic and therapeutic potency in prion-infected mice, with the lead compound extending survival by greater than80% and showing activity against both mouse and hamster prions as well as efficacy upon intraperitoneal administration into mice. These results demonstrate the feasibility of targeted chemical design of compounds that may be useful for treating diseases of aberrant protein aggregation such as prion disease.

  • 5.
    Rusakiewicz, Sylvie
    et al.
    Institut Gustave Roussy (IGR), Villejuif, France .
    Nocturne, Gaetane
    Université Paris-Sud, Le Kremlin Bicêtre, France.
    Lazure, Thierry
    Hôpitaux Universitaires Paris-Sud, Le Kremlin Bicêtre, France. .
    Semeraro, Michaela
    Institut Gustave Roussy (IGR), Villejuif, France .
    Flament, Caroline
    Institut Gustave Roussy (IGR), Villejuif, France .
    Caillat-Zucman, Sophie
    Hôpital St-Vincent de Paul, Paris, France.
    Sene, Damien
    Hôpital St-Vincent de Paul, Paris, France.
    Delahaye, Nicolas
    Institut Gustave Roussy (IGR), Villejuif, France .
    Vivier, Eric
    Centre d'Immunologie Marseille Luminy, INSERM, U1104, France.
    Chaba, Kariman
    Institut Gustave Roussy (IGR), Villejuif, France .
    Poirier-Colame, Vichnou
    Institut Gustave Roussy (IGR), Villejuif, France .
    Nordmark, Gunnel
    Uppsala University, Sweden .
    Eloranta, Maija-Leena
    Uppsala University, Sweden .
    Eriksson, Per
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Rheumatology.
    Theander, Elke
    Skåne University Hospital, Lund University, Malmö, Sweden.
    Forsblad-dElia, Helena
    Sahlgrenska Academy at University of Gothenburg, Sweden.
    Omdal, Roald
    Stavanger University Hospital, Norway .
    Wahren-Herlenius, Marie
    Karolinska Institutet, Stockholm, Sweden.
    Jonsson, Roland
    University of Bergen, Norway .
    Rönnblom, Lars
    Uppsala University, Sweden .
    Nititham, Joanne
    University of California, San Francisco, USA .
    Taylor, Kimberly E.
    University of California, San Francisco, USA .
    Lessard, Christopher J.
    University of Oklahoma Health Sciences Center, Oklahoma City, USA .
    Moser Sivils, Kathy L.
    University of Oklahoma Health Sciences Center, Oklahoma City, USA .
    Gottenberg, Jacques-Eric
    Strasbourg University Hospital, France .
    Criswell, Lindsey A.
    University of California, San Francisco, USA .
    Miceli-Richard, Corinne
    Institut Gustave Roussy (IGR), Villejuif, France .
    Zitvogel, Laurence
    Institut Gustave Roussy (IGR), Villejuif, France .
    Mariette, Xavier
    Université Paris-Sud, Le Kremlin Bicêtre, France.
    NCR3/NKp30 Contributes to Pathogenesis in Primary Sjögren’s Syndrome2013In: Science Translational Medicine, ISSN 1946-6234, E-ISSN 1946-6242, Vol. 5, no 195Article in journal (Refereed)
    Abstract [en]

    Primary Sjögrens syndrome (pSS) is a chronic autoimmune disease characterized by a lymphocytic exocrinopathy. However, patients often have evidence of systemic autoimmunity, and they are at markedly increased risk for the development of non-Hodgkins lymphoma. Similar to other autoimmune disorders, a strong interferon (IFN) signature is present among subsets of pSS patients, although the precise etiology remains uncertain. NCR3/NKp30 is a natural killer (NK)-specific activating receptor regulating the cross talk between NK and dendritic cells and type II IFN secretion. We performed a case-control study of genetic polymorphisms of the NCR3/NKp30 gene and found that rs11575837 (Gandgt;A) residing in the promoter was associated with reduced gene transcription and function as well as protection to pSS. We also demonstrated that circulating levels of NCR3/NKp30 were significantly increased among pSS patients compared with controls and correlated with higher NCR3/NKp30 but not CD16-dependent IFN-gamma secretion by NK cells. Excess accumulation of NK cells in minor salivary glands correlated with the severity of the exocrinopathy. B7H6, the ligand of NKp30, was expressed by salivary epithelial cells. These findings suggest that NK cells may promote an NKp30-dependent inflammatory state in salivary glands and that blockade of the B7H6/NKp30 axis could be clinically relevant in pSS.

  • 6.
    Shalek, Alex K.
    et al.
    MIT, MA USA; Broad Institute MIT and Harvard, MA 02142 USA; Ragon Institute Massachusetts Gen Hospital MIT and Harvard, MA 02139 USA.
    Benson, Mikael
    Linköping University, Department of Clinical and Experimental Medicine, Division of Children's and Women's health. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Single-cell analyses to tailor treatments2017In: Science Translational Medicine, ISSN 1946-6234, E-ISSN 1946-6242, Vol. 9, no 408, article id eaan4730Article in journal (Other academic)
    Abstract [en]

    Single-cell RNA-seq could play a key role in personalized medicine by facilitating characterization of cells, pathways, and genes associated with human diseases such as cancer.

  • 7.
    Stafford, William C.
    et al.
    Karolinska Inst, Sweden; Obl Therapeut AB, Sweden.
    Peng, Xiaoxiao
    Karolinska Inst, Sweden; AstraZeneca, Sweden.
    Olofsson, Maria Hagg
    Karolinska Inst, Sweden; VLVBio AB, Sweden.
    Zhang, Xiaonan
    Karolinska Inst, Sweden.
    Luci, Diane K.
    NIH, MD 20892 USA.
    Lu, Li
    Karolinska Univ Hosp, Sweden.
    Cheng, Qing
    Karolinska Inst, Sweden.
    Tresaugues, Lionel
    Karolinska Inst, Sweden; Novum, Sweden.
    Dexheimer, Thomas S.
    NIH, MD 20892 USA; Michigan State Univ, MI 48824 USA.
    Coussens, Nathan P.
    NIH, MD 20892 USA; NIH, MD 20892 USA.
    Augsten, Martin
    Karolinska Inst, Sweden; Amcure GmbH, Germany; German Canc Res Ctr, Germany.
    Martinsson Ahlzen, Hanna-Stina
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Orwar, Owe
    Obl Therapeut AB, Sweden; Karolinska Inst, Sweden.
    Ostman, Arne
    Karolinska Inst, Sweden; Univ Bergen, Norway.
    Stone-Elander, Sharon
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Maloney, David J.
    NIH, MD 20892 USA; Inspyr Therapeut Inc, CA 91362 USA.
    Jadhav, Ajit
    NIH, MD 20892 USA.
    Simeonov, Anton
    NIH, MD 20892 USA.
    Linder, Stig
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Karolinska Inst, Sweden.
    Arner, Elias S. J.
    Karolinska Inst, Sweden.
    Irreversible inhibition of cytosolic thioredoxin reductase 1 as a mechanistic basis for anticancer therapy2018In: Science Translational Medicine, ISSN 1946-6234, E-ISSN 1946-6242, Vol. 10, no 428, article id eaaf7444Article in journal (Refereed)
    Abstract [en]

    Cancer cells adapt to their inherently increased oxidative stress through activation of the glutathione (GSH) and thioredoxin (TXN) systems. Inhibition of both of these systems effectively kills cancer cells, but such broad inhibition of antioxidant activity also kills normal cells, which is highly unwanted in a clinical setting. We therefore evaluated targeting of the TXN pathway alone and, more specifically, selective inhibition of the cytosolic selenocysteine-containing enzyme TXN reductase 1 (TXNRD1). TXNRD1 inhibitors were discovered in a large screening effort and displayed increased specificity compared to pan-TXNRD inhibitors, such as auranofin, that also inhibit the mitochondrial enzyme TXNRD2 and additional targets. For our lead compounds, TXNRD1 inhibition correlated with cancer cell cytotoxicity, and inhibitor-triggered conversion of TXNRD1 from an antioxidant to a pro-oxidant enzyme correlated with corresponding increases in cellular production of H2O2. In mice, the most specific TXNRD1 inhibitor, here described as TXNRD1 inhibitor 1 (TRi-1), impaired growth and viability of human tumor xenografts and syngeneic mouse tumors while having little mitochondrial toxicity and being better tolerated than auranofin. These results display the therapeutic anticancer potential of irreversibly targeting cytosolic TXNRD1 using small molecules and present potent and selective TXNRD1 inhibitors. Given the pronounced up-regulation of TXNRD1 in several metastatic malignancies, it seems worthwhile to further explore the potential benefit of specific irreversible TXNRD1 inhibitors for anticancer therapy.

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