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
FREDRIK PIEHL
Inflammation and neurodegeneration in the CNS diseases focusing on multiple sclerosis (MS)
About
Multiple sclerosis (MS) is an autoimmune disease that causes damage to the nerve fibers of the central nervous system (CNS), which is the basis for the permanent neurological disabilities that many patients eventually will develop. Inflammation also occurs in purely mechanical injuries such as traumatic brain injury, which may contribute to worsening of the initial nerve damage. Currently we have an incomplete understanding of how inflammation in the nervous system is regulated and what significance it may have for ensuing nerve injury.
Starting from a purely preclinical project, in which the importance of genetic factors in experimental models of nerve injury and inflammation have been identified, the program now involves translational research in both experimental preclinical models and human diseases, where the main focus is on MS.
One of the most important clinical shortcomings of current MS treatment is that while we have gained access to increasingly effective disease modulatory drugs for the initial relapsing remitting phase of MS, treatment results in later, progressive stages remain disappointing.
Within the current project we have identified biomarkers for various disease processes that reflect what happens in the blood and brain tissue. We also use experimental models to understand in what molecular processes these biomarkers are involved in. Similarly, we use biomarkers to gain insights into mechanisms of action and to monitor treatment outcomes with our disease-modulating treatments. Uniquely in Sweden a drug not formally approved for MS (Mabthera/Rituxan) has become one of the most frequently used, in part through observational data provided by us. We will now start a large national follow-up program for people newly diagnosed with MS involving all Swedish university clinics and with funding from the US foundation Pcori. The study aims to generate information on safety and efficiency of MS treatments over longer time periods than is possible in traditional randomized trials and also to engage patients in the conduction of the study to a high extent.
A side project is to study if MabThera/Rituxan is superior to traditional treatment for patients newly diagnosed with myasthenia gravis (MG), an autoimmune disease of the nerves in which inflammation disrupts the signaling between nerves and muscles. The study Rinomax, which has received support from the Medical Research Council (clinical treatment research), randomize individuals with new-onset MG to either MabThera/Rituxan or placebo. Biomarker research is also conducted in MG to better understand underlying immunological disease processes.
Research projects
-
Genetic regulation of neurodegeneration and inflammation in experimental modeler for nerve damage.
-
Identification of biomarkers in various disease stages of MS, in traumatic brain injury and psychiatric diseases.
-
Clinical treatment research in MS and MG
Selected publications
Alping P, Frisell T, Novakova L, Islam-Jakobsson P, Salzer J, Björck A, et al. Rituximab versus fingolimod after natalizumab in multiple sclerosis patients. Ann. Neurol. 2016 Jun;79(6):950-8.
Al Nimer F, Elliott C, Bergman J, Khademi M, Dring A, Aeinehband S, et al. Lipocalin-2 is increased in progressive multiple sclerosis and inhibits remyelination. Neurol Neuroimmunol Neuroinflamm 2016 Feb;3(1):e191.
Al Nimer F, Ström M, Lindblom R, Aeinehband S, Bellander B, Nyengaard J, et al. Naturally occurring variation in the Glutathione-S-Transferase 4 gene determines neurodegeneration after traumatic brain injury. Antioxid. Redox Signal. 2013 Mar;18(7):784-94.
Al Nimer F, Lindblom R, Ström M, Guerreiro-Cacais A, Parsa R, Aeinehband S, et al. Strain influences on inflammatory pathway activation, cell infiltration and complement cascade after traumatic brain injury in the rat. Brain Behav. Immun. 2013 Jan;27(1):109-22.
Swanberg M, Lidman O, Padyukov L, Eriksson P, Akesson E, Jagodic M, et al. MHC2TA is associated with differential MHC molecule expression and susceptibility to rheumatoid arthritis, multiple sclerosis and myocardial infarction. Nat. Genet. 2005 May;37(5):486-94.