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  • 1.
    Escudero-Hernández, Celia
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Bernardo, David
    Univ Valladolid, Spain.
    Arranz, Eduardo
    Univ Valladolid, Spain.
    Antonio Garrote, Jose
    Univ Valladolid, Spain; Hosp Univ Rio Hortega, Spain.
    Is celiac disease really associated with inflammatory bowel disease?2020In: Revista española de enfermedades digestivas, ISSN 1130-0108, E-ISSN 2340-4167, Vol. 112, no 1, p. 4-6Article in journal (Other academic)
    Abstract [en]

    n/a

  • 2.
    Escudero-Hernández, Celia
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences. Univ Valladolid, Spain.
    Montalvillo, Enrique
    Univ Valladolid, Spain.
    Antolin, Beatriz
    Hosp Clin Univ Valladolid, Spain.
    Bernardo, David
    Univ Valladolid, Spain.
    Antonio Garrote, Jose
    Univ Valladolid, Spain; Hosp Univ Rio Hortega, Spain.
    Arranz, Eduardo
    Univ Valladolid, Spain.
    Fernandez-Salazar, Luis
    Hosp Clin Univ Valladolid, Spain.
    Different Intraepithelial CD3(+) Cell Numbers in Crohns Disease and Ulcerative Colitis2020In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 26, no 3, p. E14-E15Article in journal (Other academic)
    Abstract [en]

    Intraepithelial immune response can be studied by flow cytometry. The proportion of CD3(+) cells differs between Crohns disease and ulcerative colitis.

    The full text will be freely available from 2020-12-28 11:12
  • 3.
    Forsberg, Anna
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Huoman, Johanna
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Inflammation and Infection. Linköping University, Faculty of Medicine and Health Sciences.
    Söderholm, Simon
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Bhai Mehta, Ratnesh
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Nilsson, Lennart
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Inflammation and Infection. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Allergy Center.
    Abrahamsson, Thomas
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Children's and Women's Health. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, H.K.H. Kronprinsessan Victorias barn- och ungdomssjukhus Linköping/Motala.
    Ernerudh, Jan
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Inflammation and Infection. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Immunology and Transfusion Medicine.
    Gustafsson, Mika
    Linköping University, Department of Physics, Chemistry and Biology, Bioinformatics. Linköping University, Faculty of Science & Engineering.
    Jenmalm, Maria
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Inflammation and Infection. Linköping University, Faculty of Medicine and Health Sciences.
    Pre- and postnatal Lactobacillus reuteri treatment alters DNA methylation of infant T helper cells2020In: Pediatric Allergy and Immunology, ISSN 0905-6157, E-ISSN 1399-3038Article in journal (Refereed)
    Abstract [en]

    Background Perinatal childhood exposures, including probiotic supplementation, may affect epigenetic modifications and impact on immune maturation and allergy development. The aim of this study was to assess the effects of pre- and postnatal Lactobacillus reuteri supplementation on DNA methylation in relation to immune maturation and allergy development. Methods DNA methylation patterns were investigated for allergy-related T helper subsets using a locus-specific method and at a genome-wide scale using the Illumina 450K array. From a randomised, double-blind, placebo-controlled allergy prevention trial with pre- and postnatal probiotic supplementation, CD4+ T helper cells were obtained at birth (from cord blood), and 12 and 24 months of age (total (placebo/probiotics); locus-specific method: CB = 32 (17/15), 12 months = 24 (9/15), 24 months = 35 (15/20); Illumina: CB = 19 (10/9), 12 months = 10 (6/4), 24 months = 19(11/8)). Results Comparing probiotics to placebo, the greatest genome-wide differential DNA methylation was observed at birth, where the majority of sites were hypomethylated, indicating transcriptional accessibility in the probiotic group. Bioinformatic analyses, including network analyses, revealed a module containing 91 genes, enriched for immune-related pathways such as chemotaxis, PI3K-Akt, MAPK and TGF-beta signalling. A majority of the module genes were associated with atopic manifestations (OR = 1.43, P = 2.4 x 10(-6)), and a classifier built on this model could predict allergy development (AUC = 0.78, P = 3.0 x 10(e-3)). Pathways such as IFN-gamma signalling and T-cell activation were more hypermethylated at birth compared with later in life in both intervention groups over time, in line with DNA methylation patterns in the IFNG locus obtained by the locus-specific methodology. Conclusion Maternal L. reuteri supplementation during pregnancy alters DNA methylation patterns in CD4+ T cells towards enhanced immune activation at birth, which may affect immune maturation and allergy development.

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  • 4.
    Fugazza, Cristina
    et al.
    Università di Milano-Bicocca, Italy.
    Barbarani, Gloria
    Università di Milano-Bicocca, Italy.
    Elangovan, Sudharshan
    Università di Milano-Bicocca, Italy.
    Marini, Maria Giuseppina
    Istituto di Ricerca Genetica e Biomedica del Consiglio Nazionale delle Ricerche, Italy.
    Giolitto, Serena
    Università di Milano-Bicocca, Italy.
    Font-Monclus, Isaura
    Università di Milano-Bicocca, Italy.
    Marongiu, Maria Franca
    Istituto di Ricerca Genetica e Biomedica del Consiglio Nazionale delle Ricerche, Italy.
    Manunza, Laura
    Universita degli Studi di Cagliari, Italy.
    Strouboulis, John
    King's College London, United Kingdom.
    Cantù, Claudio
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Gasparri, Fabio
    Nerviano Medical Sciences S.r.l., Nerviano, Italy.
    Barabino, Silvia M. L.
    Università di Milano-Bicocca, Milano, Italy.
    Nakamura, Yukio
    RIKEN BioResource Research Center, Japan.
    Ottolenghi, Sergio
    Università di Milano-Bicocca, Milano, Italy.
    Moi, Paolo
    Universita degli Studi di Cagliari, Italy.
    Ronchi, Antonella Ellena
    Università di Milano-Bicocca, Milano, Italy.
    The Coup-TFII orphan nuclear receptor is an activator of the γ-globin gene2020In: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721Article in journal (Refereed)
    Abstract [en]

    The human fetal γ-globin gene is repressed in the adult stage through complex regulatory mechanisms involving transcription factors and epigenetic modifiers. Reversing γ-globin repression, or maintaining its expression by manipulating regulatory mechanisms, has become a major clinical goal in the treatment of β-hemoglobinopathies. Here, we identify the orphan nuclear receptor Coup-TFII (NR2F2/ARP-1) as an embryonic/fetal stage activator of γ-globin expression. We show that Coup-TFII is expressed in early erythropoiesis of yolk sac origin, together with embryonic/fetal globins. When overexpressed in adult cells (including peripheral blood cells from human healthy donors and β039 thalassemic patients) Coup-TFII activates the embryonic/fetal globins genes, overcoming the repression imposed by the adult erythroid environment. Conversely, the knock-out of Coup-TFII increases the β/γ+β globin ratio. Molecular analysis indicates that Coup-TFII binds in vivo to the β-locus and contributes to its conformation. Overall, our data identify Coup-TFII as a specific activator of the γ-globin gene.

  • 5.
    Hagbom, Marie
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Meira de Faria, Felipe
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Tinnerfelt Winberg, Martin
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Westerberg, Sonja
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Nordgren, Johan
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Sharma, Sumit
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Keita, Åsa
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Loitto, Vesa
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Inflammation and Infection. Linköping University, Faculty of Medicine and Health Sciences.
    Magnusson, Karl-Eric
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Inflammation and Infection. Linköping University, Faculty of Medicine and Health Sciences.
    Svensson, Lennart
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences. Karolinska Inst, Sweden.
    Neurotrophic Factors Protect the Intestinal Barrier from Rotavirus Insult in Mice2020In: mBio, ISSN 2161-2129, E-ISSN 2150-7511, Vol. 11, no 1, article id e02834-19Article in journal (Refereed)
    Abstract [en]

    Increased intestinal permeability has been proposed as a mechanism of rotavirus-induced diarrhea. Studies with humans and mice have, however, shown that rotavirus leaves intestinal permeability unaffected or even reduced during diarrhea, in contrast to most bacterial infections. Gastrointestinal permeability is regulated by the vagus nerve and the enteric nervous system, which is composed of neurons and enteric glial cells (EGCs). We investigated whether the vagus nerve, serotonin (5-HT), EGCs, and neurotropic factors contribute to maintaining gut barrier homeostasis during rotavirus infection. Using subdiaphragmatic vagotomized and 5-HT3 receptor knockout mice, we found that the unaffected epithelial barrier during rotavirus infection is independent of the vagus nerve but dependent on 5-HT signaling through enteric intrinsic 5-HT3 receptors. Immunofluorescence analysis showed that rotavirus-infected enterocytes were in close contact with EGCs and enteric neurons and that the glial cell-derived neurotrophic factor (GDNF) was strongly upregulated in enterocytes of infected mice. Moreover, rotavirus and 5-HT activated EGCs (P < 0.001). Using Ussing chambers, we found that GDNF and S-nitrosoglutathione (GSNO) led to denser epithelial barriers in small intestinal resections from noninfected mice (P < 0.01) and humans (P < 0.001) and that permeability was unaffected in rotavirus-infected mice. GSNO made the epithelial barrier denser in Caco-2 cells by increasing the expression of the tight junction protein zona occludens 1 (P < 0.001), resulting in reduced passage of fluorescein isothiocyanate dextran (P < 0.05) in rotavirus-infected monolayers. This is the first report to show that neurotropic factors contribute to maintaining the gut epithelial barrier during viral insult. IMPORTANCE Human and mouse studies have shown that rotavirus infection is associated with low inflammation and unaffected intestinal barrier at the time of diarrhea, properties different from most bacterial and inflammatory diseases of the gut. We showed by in vitro, ex vivo, and in vivo experiments that neurotrophic factors and 5-HT have barrier protective properties during rotavirus insult. These observations advance our understanding of how the gut barrier is protected against rotavirus and suggest that rotavirus affects the gut barrier differently from bacteria. This is the first report to show that neurotrophic factors contribute to maintain the gut epithelial barrier during viral insult.

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  • 6.
    Keita, Åsa
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Yakimenko Alkaissi, Lina
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Boström Holm, Elin
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Heil, Stéphanie
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Chassaing, Benoit
    Georgia State Univ, GA 30303 USA; Georgia State Univ, GA 30303 USA.
    Darfeuille-Michaud, Arlette
    Univ Auvergne, France.
    McKay, Derek M.
    Univ Calgary, Canada.
    Söderholm, Johan D
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Surgery in Linköping.
    Enhanced E. coli LF82 Translocation through the Follicle-associated Epithelium in Crohns Disease is Dependent on Long Polar Fimbriae and CEACAM6 expression, and Increases Paracellular Permeability2020In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 14, no 2, p. 216-229Article in journal (Refereed)
    Abstract [en]

    Background and Aims: Patients with Crohns disease [CD] harbour an increased number of adherent-invasive E. coli [AIEC]. The strain LF82, identified in the ileal mucosa of CD patients, has been extensively studied for pathogenic mechanisms. However, understanding of the interaction of LF82 with the intestinal mucosa of CD patients is lacking. Methods: Here, we investigated the importance of long polar fimbriae [LPF] type 1 pili and the carcinoembryonic antigen-related cell-adhesion molecule 6 [CEACAM6] for translocation of LF82 in an in vitro model of follicle-associated epithelium [FAE], and in the FAE and villus epithelium [VE] of patients with CD and controls, using Ussing chambers. Results: Significantly greater LF82 passage occurred in the FAE model compared with in the VE Caco-2cl1 mono-culture. Moreover, bacterial translocation was inhibited by either LPF disruption or pre-incubation with anti-CEACAM6 antibody. Tissue mounted in Ussing chambers showed significantly higher LF82 passage in FAE from patients with CD compared with control FAE, that was diminished in LF82 lacking LPF and by blocking host CEACAM6. Interestingly, addition of LF82 to the CD FAE tissues significantly increased paracellular permeability [of (51)Chromium-EDTA] compared with baseline, and the increase was inhibited by anti-CEACAM6. Immunofluorescence and immunoblots showed higher expression of CEACAM6 in FAE of patients with CD compared with in FAE from controls. Conclusions: These data suggest that the FAE of CD patients is a site of vulnerability for invasion by LF82 via a mechanism that requires both bacterial LPF and host CEACAM6. Further, LF82 has the ability to increase paracellular passage through the FAE of patients with CD. These data can help define novel therapeutic targets in CD for the prevention of clinical recurrence.

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  • 7.
    Magnusson, Louise
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Children's and Women's Health. Linköping University, Faculty of Medicine and Health Sciences. Uppsala Univ, Sweden.
    Barcenilla, Hugo
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Children's and Women's Health. Linköping University, Faculty of Medicine and Health Sciences.
    Pihl, Mikael
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Bensing, Sophie
    Karolinska Inst, Sweden.
    Espes, Daniel
    Uppsala Univ, Sweden; Uppsala Univ, Sweden.
    Carlsson, Per-Ola
    Uppsala Univ, Sweden; Uppsala Univ, Sweden.
    Casas, Rosaura
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Children's and Women's Health. Linköping University, Faculty of Medicine and Health Sciences.
    Mass Cytometry Studies of Patients With Autoimmune Endocrine Diseases Reveal Distinct Disease-Specific Alterations in Immune Cell Subsets2020In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 11, article id 288Article in journal (Refereed)
    Abstract [en]

    Although there is evidence that autoimmune diseases share similar immunogenetic mechanisms, studies comparing peripheral CD45(+) cells from patients with autoimmune endocrine diseases in parallel are limited. In this study, we applied high-dimensional single-cell mass cytometry to phenotypically characterize PBMC from patients with new-onset (N-T1D) and long-standing type 1 diabetes, Hashimotos thyroiditis (HT), Graves disease and autoimmune Addisons disease (AD), as well as healthy controls. The frequency of CD20(lo)CD27(hi)CD38(hi)HLA-DRint plasmablasts, CD86(+)CD14(lo)CD16(+) non-classical monocytes and two subsets of CD56(dim)HLA-DR+IFN-gamma(+) NK cells were increased in patients with HT. Subsets of CD56(dim)CD69(+)HLA-DR- NK cells and CD8(+) TEMRA cells, both expressing IFN-gamma, were expanded and reduced, respectively, in the N-T1D group. In addition, patients with AD were characterized by an increased percentage of central memory CD8(+) T cells that expressed CCR4, GATA3, and IL-2. We demonstrate that patients with N-T1D, HT, and AD had altered frequencies of distinct subsets within antigen-presenting and cytotoxic cell lineages. Previously unreported alterations of specific cell subsets were identified in samples from patients with HT and AD. Our study might contribute to a better understanding of shared and diverging immunological features between autoimmune endocrine diseases.

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  • 8.
    Phillips, C.
    et al.
    Univ Santiago de Compostela, Spain.
    Amigo, J.
    IDIS, Spain.
    Tillmar, Andreas
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences. Natl Board Forens Med, Dept Forens Genet and Forens Toxicol, Linkoping, Sweden.
    Peck, M. A.
    Int Commiss Missing Persons, Netherlands.
    de la Puente, M.
    Univ Santiago de Compostela, Spain.
    Ruiz-Ramirez, J.
    Univ Santiago de Compostela, Spain.
    Bittner, F.
    Int Commiss Missing Persons, Netherlands.
    Idrizbegovic, S.
    Int Commiss Missing Persons, Netherlands.
    Wang, Y.
    Qiagen, MD 21703 USA.
    Parsons, T. J.
    Int Commiss Missing Persons, Netherlands.
    Lareu, M. V.
    Univ Santiago de Compostela, Spain.
    A compilation of tri-allelic SNPs from 1000 Genomes and use of the most polymorphic loci for a large-scale human identification panel2020In: Forensic Science International: Genetics, ISSN 1872-4973, E-ISSN 1878-0326, Vol. 46, article id UNSP 102232Article in journal (Refereed)
    Abstract [en]

    In a directed search of 1000 Genomes Phase III variation data, 271,934 tri-allelic single nucleotide polymorphisms (SNPs) were identified amongst the genotypes of 2,504 individuals from 26 populations. The majority of tri-allelic SNPs have three nucleotide substitution-based alleles at the same position, while a much smaller proportion, which we did not compile, have a nucleotide insertion/deletion plus substitution alleles. SNPs with three alleles have higher discrimination power than binary loci but keep the same characteristic of optimum amplification of the fragmented DNA found in highly degraded forensic samples. Although most of the tri-allelic SNPs identified had one or two alleles at low frequencies, often single observations, we present a full compilation of the genome positions, rs-numbers and genotypes of all tri-allelic SNPs detected by the 1000 Genomes project from the more detailed analyses it applied to Phase III sequence data. A total of 8,705 tri-allelic SNPs had overall heterozygosities (averaged across all 1000 Genomes populations) higher than the binary SNP maximum value of 0.5. Of these, 1,637 displayed the highest average heterozygosity values of 0.6-0.666. The most informative tri-allelic SNPs we identified were used to construct a large-scale human identification panel for massively parallel sequencing, designed for the identification of missing persons. The large-scale MPS identification panel comprised: 1,241 autosomal tri-allelic SNPs and 29 X tri-allelic SNPs (plus 46 microhaplotypes adapted for genotyping from reduced length sequences). Allele frequency estimates are detailed for African, European, South Asian and East Asian population groups plus the Peruvian population sampled by 1000 Genomes for the 1,270 tri-allelic SNPs of the final MPS panel. We describe the selection criteria, kinship simulation experiments and genomic analyses used to select the tri-allelic SNP components of the panel. Approximately 5 % of the tri-allelic SNPs selected for the large-scale MPS identification panel gave three-genotype patterns in single individual samples or discordant genotypes for genomic control DNAs. A likely explanation for some of these unreliably genotyped loci is that they map to multiple sites in the genome - high-lighting the need for caution and detailed scrutiny of multiple-allele variant data when designing future forensic SNP panels, as such patterns can arise from common structural variation in the genome, such as segmental duplications.

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  • 9.
    Sharma, Sumit
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Hagbom, Marie
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Svensson, Lennart
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences. Karolinska Inst, Sweden.
    Nordgren, Johan
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    The Impact of Human Genetic Polymorphisms on Rotavirus Susceptibility, Epidemiology, and Vaccine Take2020In: VIRUSES-BASEL, Vol. 12, no 3, article id 324Article, review/survey (Refereed)
    Abstract [en]

    Innate resistance to viral infections can be attributed to mutations in genes involved in the immune response, or to the receptor/ligand. A remarkable example of the latter is the recently described Mendelian trait resistance to clinically important and globally predominating genotypes of rotavirus, the most common agent of severe dehydrating gastroenteritis in children worldwide. This resistance appears to be rotavirus genotype-dependent and is mainly mediated by histo-blood group antigens (HBGAs), which function as a receptor or attachment factors on gut epithelial surfaces. HBGA synthesis is mediated by fucosyltransferases and glycosyltransferases under the genetic control of the FUT2 (secretor), FUT3 (Lewis), and ABO (H) genes on chromosome 19. Significant genotypic and phenotypic diversity of HBGA expression exists between different human populations. This genetic diversity has an effect on genotype-specific susceptibility, molecular epidemiology, and vaccine take. Here, we will discuss studies on genetic susceptibility to rotavirus infection and place them in the context of population susceptibility, rotavirus epidemiology, vaccine take, and public health impact.

  • 10.
    Tillmar, Andreas
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences. Natl Board Forens Med, Dept Forens Genet and Forens Toxicol, Linkoping, Sweden.
    Sjolund, Peter
    Peter Sjolund AB, Sweden.
    Lundqvist, Bo
    Swedish Police Author, Sweden.
    Klippmark, Therese
    Natl Board Forens Med, Dept Forens Genet and Forens Toxicol, Linkoping, Sweden.
    Algenas, Cajsa
    Natl Board Forens Med, Dept Forens Genet and Forens Toxicol, Linkoping, Sweden.
    Green, Henrik
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Natl Board Forens Med, Dept Forens Genet and Forens Toxicol, Linkoping, Sweden.
    Whole-genome sequencing of human remains to enable genealogy DNA database searches - A case report2020In: Forensic Science International: Genetics, ISSN 1872-4973, E-ISSN 1878-0326, Vol. 46, article id UNSP 102233Article in journal (Refereed)
    Abstract [en]

    Recently a number of high profile crime cases (e.g. the "Golden State Killer") have successfully been solved or given new leads with the use of genome wide DNA data in combination with pairwise matching from individuals present in genealogy DNA databases. Such databases will primarily involve distant relatives which in turn require a large amount of genetic information, in the range of several hundred thousand to millions of SNPs, to be genotyped. While it nowadays is fairly straightforward to obtain such as data from high quality and high quantity DNA, it is still a challenge for degraded DNA of low quantity such in the case of forensic samples. Here we present a successful effort in obtaining genome-wide genotype data from human remains. The goal was to get investigative leads in order to identify the remains of an unknown male ("the Ekeby man") that was found murdered in the south of Sweden in 2003. Whole-genome sequencing was performed on DNA originating from a bone sample. Three replicates of libraries were prepared using ThruPLEX DNA-seq Kit (Takara) which were sequenced on a HiSeq X instrument (Illumina). A mean coverage of 30X was obtained when the sequencing reads were mapped to a human reference genome. Following further bioinformatic processing, allele calling, quality checks and filtering to match the genealogy DNA database SNPs, genotypes for approximately one million SNPs were established. The resulting SNP genotypes were then used to search for relatives in the genealogy DNA database GEDmatch (www.gedmatch.com). A candidate list of relatives was obtained which was further processed using traditional genealogy methods in order to get leads about the identity of the unknown. In summary, this report shows how whole-genome sequencing successfully can be applied on forensic samples to create the SNP genotypes required for searches in genealogy DNA databases for the purpose of generating leads to identify missing or unknown persons, including perpetrators and victims.

  • 11.
    Åhsberg, Josefine
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Xiao, Pingnan
    Karolinska Inst, Sweden.
    Okuyama, Kazuki
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Somasundaram, Rajesh
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Strid, Tobias
    Lund Univ, Sweden.
    Qian, Hong
    Lund Univ, Sweden.
    Sigvardsson, Mikael
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences. Lund Univ, Sweden.
    Letter: Progression of progenitor B-cell leukemia is associated with alterations of the bone marrow micro-environment in HAEMATOLOGICA, vol 105, issue 3, pp2020In: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 105, no 3Article in journal (Other academic)
    Abstract [en]

    n/a

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