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  • 1.
    Bozorg, Soran Rabin
    et al.
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm Sweden.
    Söderling, Jonas
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden.
    Everhiv, Åsa H.
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden; Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.
    Lebwohl, Benjamin
    Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA.
    Green, Peter H. R.
    Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA.
    Neovius, Martin
    Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm Sweden; Celiac Disease Center, Department of Medicine, Columbia University Medical Centre, Columbia University, New York, USA; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Mårild, Karl
    Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, Gothenburg, Sweden; Department of Pediatric Gastroenterology, Queen Silvia Children’s Hospital, Gothenburg, Sweden.
    Work loss before and after diagnosis in patients with celiac disease2021In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 51, no Suppl. 1, p. 286-286Article in journal (Other academic)
    Abstract [en]

    Celiac disease (CD) is an immune‐mediated disease triggered by gluten intake and affects around 1% of the population worldwide. Although patients with CD have an increased use of healthcare, data on work disability remains scarce. To estimate work loss in patients with CD before and after diagnosis. We identified 16,005 working‐age patients with prevalent CD, and 4,936 incident working‐age patients diagnosed in 2008‐2015 through biopsy reports from Sweden’s 28 pathology departments. CD was defined by presence of villus atrophy (Marsh 3) on biopsy (gold standard). Each patient was compared to up to 5 matched general‐population comparators. Using nationwide social insurance registers, we retrieved prospectively‐recorded data on compensation for sick leave and disability. In 2015, patients with prevalent CD had a mean of 42.5 (95%CI: 40.9‐44.1) lost work days as compared with 28.6 (27.9‐29.2) in the general‐population comparators, corresponding to a relative difference of 49%. Among incident patients, the annual mean difference between patients and comparators was 8.0 (5.4‐10.6) lost work days 5 years before CD diagnosis, which grew to 13.7 (9.1‐18.3) days 5 years after diagnosis. In addition to the continuously increasing mean difference in lost work days over time, there was also a transient increase in work loss in patients with CD during the year of diagnosis (mean difference: 15.6 days, 95%CI: 13.1‐18.0). Patients with CD miss more work days than comparators before their diagnosis, and this loss increases and persists after diagnosis despite presumed installation of treatment with gluten‐free diet. 

  • 2.
    Degen, Winfried G. J.
    et al.
    Department of Biochemistry, University of Nijmegen, Nijmegen, The Netherlands.
    Pieffers, Martijn
    Department of Biochemistry, University of Nijmegen, Nijmegen, The Netherlands.
    Welin-Henriksson, Elisabet
    Department of Medicine, Rheumatology Research Unit, Center for Molecular Medicine, Karolinska Institutet & Karolinska Hospital, Stockholm, Sweden.
    van den Hoogen, Frank H. J.
    Department of Rheumatology, University Hospital Nijmegen, Nijmegen, The Netherlands.
    van Venrooij, Walther J.
    Department of Biochemistry, University of Nijmegen, Nijmegen, The Netherlands.
    Raats, Jos M. H.
    Department of Biochemistry, University of Nijmegen, Nijmegen, The Netherlands.
    Characterization of recombinant human autoantibody fragments directed toward the autoantigenic U1-70K protein2000In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 30, no 10, p. 3029-3038Article in journal (Refereed)
    Abstract [en]

    The U1-70K protein is specifically bound to stemloop I of the U1 small nuclear RNA contained in the U1 small nuclear ribonucleoprotein complex (U1 snRNP), which is involved in the splicing of pre-mRNA. All components of the U1 snRNP complex, including the U1-70K protein, are important autoantigens in patients with systemic lupus erythematosus (SLE) and mixed connective tissue disease (MCTD). Here we describe for the first time the selection and characterization of recombinant human anti-U1-70K single chain autoantibody fragments (anti-hU1-70K scFv) from autoimmune patient-derived phage display antibody libraries. All scFv specifically recognize parts of the hU1-70K protein and its apoptotic 40-kDa cleavage product. In Western blotting assays a number of scFv preferentially recognize the 40-kDa apoptotic cleavage fragment of the U1-70K protein, suggesting a possible involvement of this apoptotic cleavage product in the autoimmune response of patients. The germline gene usage of these recombinant autoantibodies was also determined. Using several U1-70K deletion and point mutants of both human (h) and Drosophila melanogaster (Dm) origin, it was established that the U1-70K epitope that is recognized by the anti-hU1-70K scFv is located within the RNA binding domain.

  • 3.
    Kumawat, Ashok Kumar
    et al.
    Örebro University, School of Medical Sciences. Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, UK.
    Yu, Chen
    Department of Biological Sciences, Center for Cancer, Genetic Diseases and Gene Regulation, Fordham University, Bronx NY, USA.
    Mann, Elizabeth A.
    Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, UK.
    Schridde, Anika
    Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, UK.
    Finnemann, Silvia C.
    Department of Biological Sciences, Center for Cancer, Genetic Diseases and Gene Regulation, Fordham University, Bronx NY, USA.
    Mowat, Allan McI
    Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, UK.
    Expression and characterization of αvβ5 integrin on intestinal macrophages2018In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 48, no 7, p. 1181-1187Article in journal (Refereed)
    Abstract [en]

    Macrophages play a crucial role in maintaining homeostasis in the intestine, but the underlying mechanisms have not yet been elucidated fully. Here we show for the first time that mature intestinal macrophages in mouse colon and small intestine express high levels of αvβ5 integrin, which acts as a receptor for the uptake of apoptotic cells and can activate molecules involved in several aspects of tissue homeostasis such as angiogenesis and remodelling of the extracellular matrix. αvβ5 is not expressed by other immune cells in the intestine, is already present on intestinal macrophages soon after birth, and its expression is not dependent on the microbiota. In adults, αvβ5 induces the differentiation of monocytes in response to the local environment and it confers intestinal macrophages with the ability to promote engulfment of apoptotic cells via engagement of the bridging molecule milk fat globule EGF-like molecule 8. In the absence of αvβ5, there are fewer monocytes in the mucosa and mature intestinal macrophages have decreased expression of metalloproteases and interleukin 10. Mice lacking αvβ5 on haematopoietic cells show increased susceptibility to chemical colitis and we conclude that αvβ5 contributes to the tissue repair by regulating the homeostatic properties of intestinal macrophages.

  • 4.
    Laajala, Essi
    et al.
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, Turku, Finland; Turku Doctoral Programme of Molecular Medicine, University of Turku, Turku, Finland; Department of Computer Science, Aalto University, Espoo, Finland .
    Ullah, Ubaid
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, Turku, Finland .
    Grönroos, Toni
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, Turku, Finland .
    Rasool, Omid
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, Turku, Finland .
    Aho, Viivi Halla
    Department of Computer Science, Aalto University, Espoo, Finland .
    Konki, Mikko
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Kattelus, Roosa
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, Turku, Finland .
    Mykkänen, Juha
    Research Centre of Applied and Preventive Cardiovascular Medicine, Institute of Biomedicine, University of Turku, Turku, Finland .
    Nurmio, Mirja
    Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland.
    Mäkilä, Mari Vahä
    Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland.
    Kallionpää, Henna
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Lietzén, Niina
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Laiho, Asta
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Hyöty, Heikki
    Department of Virology, Faculty of Medicine and Biosciences, University of Tampere, Tampere, Finland.
    Elo, Laura L.
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, Turku, Finland .
    Ilonen, Jorma
    Immunogenetics Laboratory, Institute of Biomedicine, University of Turku, Turku, Finland .
    Knip, Mikael
    Pediatric Research Center, Children’s Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland; Center for Child Health Research, Tampere University Hospital, Tampere, Finland.
    Lund, Riikka J.
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Oresic, Matej
    Örebro University, School of Medical Sciences. Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.
    Veijola, Riitta
    Department of Pediatrics, PEDEGO Research Unit, Medical Research Centre, Oulu, Finland.
    Lähdesmäki, Harri
    Department of Computer Science, Aalto University, Espoo, Finland .
    Toppari, Jorma
    Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland; Department of Pediatrics, Turku University Hospital, Turku, Finland; Centre for Population Health Research, University of Turku and Turku University Hospital, Turku, Finland .
    Lahesmaa, Riitta
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, Turku, Finland .
    Umbilical cord blood DNA methylation in children who later develop type 1 diabetes2021In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 51, no Suppl. 1, p. 291-291Article in journal (Other academic)
    Abstract [en]

    Distinct DNA methylation patterns have recently been observed to precede Type 1 Diabetes in whole blood collected from young children. Our aim was to determine if such methylation patterns are present already at the time of birth. Reduced representation bisulfite sequencing (RRBS) analysis was performed on a unique collection of umbilical cord blood samples collected within the Type 1 Diabetes Prediction and Prevention (DIPP) study. Children later diagnosed with Type 1 Diabetes and/or testing positive for multiple islet autoantibodies (N=43) were compared to control individuals (N=79), who remained autoantibody‐negative throughout the DIPP follow‐up until 15 years of age. Altogether 24 clinical and technical covariates related to the pregnancy and the mother were included in a binomial mixed effects model, which was fit separately for each high‐coverage CpG site, followed by spatial and multiple testing adjustment of P values. We discovered a strong inflation of P values, which was caused by a standard spatial adjustment method. Findings that were based on Benjamini‐Hochberg corrected spatially adjusted P values, could not be validated by Pyrosequencing. We therefore used permutation‐based significance analysis and showed that sex‐associated differentially methylated cytosines could be reproducibly detected with this approach. After empirical type 1 error control, no differences in cord blood methylation patterns were observed between cases and controls. Differences between children who progress to Type 1 Diabetes and those who remain healthy throughout childhood, are not yet present in the perinatal DNA methylome.

  • 5.
    Papapavlou, Georgia
    et al.
    Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Hellberg, Sandra
    Division of Bioinformatics, Department of Physics, Chemistry and Biology, Linköping University, Linköping, Sweden.
    Raffetseder, Johanna
    Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Brynhildsen, Jan
    Örebro University, School of Medical Sciences. Department of Obstetrics and Gynecology, and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden; Department of Obstetrics and Gynecology, Faculty of Medicine, Örebro University, Örebro, Sweden.
    Gustafsson, Mika
    Division of Bioinformatics, Department of Physics, Chemistry and Biology, Linköping University, Linköping, Sweden.
    Jenmalm, Maria C.
    Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Ernerudh, Jan
    Department of Clinical Immunology and Transfusion Medicine, and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Differential effects of estradiol and progesterone on human T cell activation in vitro2021In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 51, no 10, p. 2430-2440Article in journal (Refereed)
    Abstract [en]

    Estradiol (E2) and progesterone (P4) are steroid hormones important for the regulation of immune responses during pregnancy. Their increasing levels coincide with an improvement of T cell-mediated diseases such as multiple sclerosis (MS). Although immune-endocrine interactions are involved in this phenomenon, the relative contribution of hormones is not known. We here report a direct comparison of E2- and P4-mediated effects on human CD4+ T cells, key cells in immune regulation. T cells were stimulated to obtain different activation levels and exposed to a broad range of hormone concentrations. Activation level was assessed by CD69/CD25 expression by flow cytometry, and secreted proteins (n = 196) were measured in culture supernatants using proximity extension assay and electrochemiluminescence immunoassay. We found that in low activated cells, pregnancy-relevant E2 concentrations increased activation and the secretion of several immune- and inflammation-related proteins. P4, on the other hand, showed a biphasic pattern, where serum-related concentrations upregulated activation and protein secretion while placenta-relevant concentrations induced a prominent dampening irrespective of the initial activation level. Our results demonstrate the importance of P4 as a major hormone in the immune modulation of T cells during pregnancy and emphasize the need to further evaluate its potency in the treatment of diseases like MS.

  • 6.
    Sen, Partho
    et al.
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Andrabi, Syed Bilal Ahmad
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
    Buchacher, Tanja
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
    Khan, Mohd Moin
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
    Ullah, Ubaid
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
    Lindeman, Tuomas Mikael
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Alves, Marina Amaral
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Hinkkanen, Victoria
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Kemppainen, Esko
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Dickens, Alex M.
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Rasool, Omid
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
    Hyötyläinen, Tuulia
    Örebro University, School of Science and Technology. Department of Chemistry.
    Lahesmaa, Riitta
    Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
    Oresic, Matej
    Örebro University, School of Medical Sciences. Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland .
    Quantitative analysis of human CD4+T-cell differentiation reveals subset-specific regulation of glycosphingolipid pathways2021In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 51, no Suppl. 1, p. 237-237Article in journal (Other academic)
    Abstract [en]

    T‐cells are sentinels of adaptive immune responses. T‐cell activation, proliferation and differentiation involves metabolic reprogramming involving the interplay of genes, proteins and metabolites. Here, we aim to understand the metabolic pathways involved in the activation and functional differentiation of human CD4+ T‐cell subsets (Th1, Th2, Th17 and iTregs). We combined genome‐scale metabolic modeling, gene expression data, targeted and non‐targeted lipidomics experiments, together with in vitro gene knockdown experiments and showed that human CD4+ T cells undergo specific metabolic changes during activation and functional differentiation. In addition, we identified and confirmed the importance of ceramide and glycosphingolipid biosynthesis pathways in Th17 differentiation and effector functions. Through in vitro gene knockdown experiments, we substantiated the requirement of serine palmitoyl transferase, a de novo sphingolipid pathway in the expression of proinflammatory cytokine (IL17A and IL17F) by Th17 cells. Our findings may provide a comprehensive resource for identifying CD4+ T‐cell‐specific targets for their selective manipulation under disease conditions, particularly, diseases characterized by an imbalance of Th17/nTreg cells. 

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