Biography
Professor Robert A. Harris
Professor Robert A. Harris (Bob) was born in Harpenden in Southern UK in 1966. He conducted a Bsc.Hons undergraduate degree at Portsmouth Polytechnic, majoring in Parasitology in 1987. PhD studies at University College London studying innate immune agglutinins in Schistosoma host snail species with Terry Preston and Vaughan Southgate as supervisors culminated with a thesis defence in early 1991. A 2.5 year postdoc at the London School of Hygiene & Tropical Medicine in Paul Kaye’s research group ensued, with focus on understanding the intracellular fate of Leishmania spp. protozoans in macrophages. Bob was awarded a Wellcome Trust postdoctoral fellowship that permitted his relocation to the Karolinska Institutet (Stockholm, Sweden) in the spring of 1994. A postdoc period was spent split between the labs of Anders Örn and Tomas Olsson, in which he studied Trypanosoma cruzi and Trypanosoma bruceii protozoan proteins. Bob became an Associate Professor at the Karolinska Institutet in 1999, heralding his establishment as a PI. Bob started to work with autoimmune diseases in 1996 and began study of therapy using live parasite infections or parasite molecules. His research group has developed autoantigen-specific vaccines, defined the effects of post-translational biochemical molecules on autoantigenicity and developed a macrophage adoptive transfer therapy that prevents pathogenesis in several experimental disease models. He became Professor of Immunotherapy in Neurological Diseases in 2013. In recent years research focus has centred on understanding the immunopathogenesis of incurable neurodegenerative diseases, with particular emphasis on development of immunotherapies directed at microglial cells as potential therapeutic paradigms.
Bob Harris CV July 2020
ERIK HERLENIUS GROUP
Development of autonomic control
About
Immature or deficient autonomic control is a common problem in infants born at a premature age and is of central importance in apneas, secondary hypoxic brain damage and sudden infant death syndrome.
PER ERIKSSON GROUP
Research
For better understanding of disturbances in respiratory control we study early development of cardiorespiratory control, brainstem neural networks and its associations with normal and pathological breathing. The conceptual change introduced by our recent data that endogenous prostaglandins are central pathogenic factors in respiratory disorders and the hypoxic response, open new diagnostic and therapeutic avenues that should significantly better the diagnostics and treatment of newborns and adult patients.
Inflammation is a major culprit in breathing disorders and we hypothesize that by using a newly developed urinary prostaglandin biomarker we can screen, detect and protect against inflammation related breathing disorders.
Our collaborative efforts enable us to move from a clinical problem to molecular understanding of the disease and studies are performed in patients, animal & in vitro models.
Our research is focused on the development of autonomic control with normal and paediatric patients as the target. Autonomic dysfunction in breathing and circulatory control often has its origin in neurodevelopment disorders. Furthermore, our basic research in developmental neuroscience how neural activity and stem cells form activity dependent networks is vital for the development of therapeutic interventions.
Read more
Contact: communication@cmm.se
CENTER FOR MOLECULAR MEDICINE
Medical epigenetics
TOMAS EKSTRÖM TEAM
About
The genetic material, or genome, which is identical in all cells of an individual, is composed of DNA and associated proteins, which together make up the chromatin. Chromatin is nessecary for the packaging of the genetic material in every cell nucleus of the organism, as well as for the regulation of gene programs, which are different in all cell types and which can be altered in disease. This is done partly by employing epigenetic mechanisms.
We are studying the integration between these mechanisms, the genome and environmental exposures in order to understand risks of autoimmune inflammatory chronic diseases that affect 1/3 of the Swedish population, a great burdon on individuals and society. The coordination of the genome with the epigenetic make-up is likely of great importance.
Rheumatoid arthritis (RA), a systemic inflammatory disease primarily affecting the flexible joints, and multiple sclerosis (MS), a neurological disease affecting the function of nerves in the central nervous system, are both chronic autoimmune diseases associated with inflammation.
Our research is connecting individual epigenetic profiles with genetic background, lifestyle and disease risks. We try to find epigenetic molecular causes to why individuals with certain genetic make-up combined with certain environmental exposures are affected by RA or MS, and why therapy responses are different among affected individuals. To achieve this, we use advanced technology and bioinformatics with clinical patient material.
Selected publications
Almgren M, Schlinzig T, Gomez-Cabrero D, Gunnar A, Sundin M, Johansson S, et al. Cesarean delivery and hematopoietic stem cell epigenetics in the newborn infant: implications for future health? Am. J. Obstet. Gynecol. 2014 Nov;211(5):502.e1-8.
Liu Y, Aryee M, Padyukov L, Fallin M, Hesselberg E, Runarsson A, et al. Epigenome-wide association data implicate DNA methylation as an intermediary of genetic risk in rheumatoid arthritis. Nat. Biotechnol. 2013 Feb;31(2):142-7.
Esteki-Zadeh A, Karimi M, Strååt K, Ammerpohl O, Zeitelhofer M, Jagodic M, et al. Human cytomegalovirus infection is sensitive to the host cell DNA methylation state and alters global DNA methylation capacity. Epigenetics 2012 Jun;7(6):585-93.
Melas P, Rogdaki M, Ösby U, Schalling M, Lavebratt C, Ekström T. Epigenetic aberrations in leukocytes of patients with schizophrenia: association of global DNA methylation with antipsychotic drug treatment and disease onset. FASEB J. 2012 Jun;26(6):2712-8.
Arzenani M, Zade A, Ming Y, Vijverberg S, Zhang Z, Khan Z, et al. Genomic DNA hypomethylation by histone deacetylase inhibition implicates DNMT1 nuclear dynamics. Mol. Cell. Biol. 2011 Oct;31(19):4119-28.