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
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
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.
CENTER FOR MOLECULAR MEDICINE
MARINA KOROTKOWA TEAM
Lipid mediators in rheumatic diseases: novel means of regulation
Lipid mediators have an important role in the pathogenesis of rheumatic diseases, and enzymes and receptors involved in lipid mediator biosynthesis or action constitute valuable therapeutic targets. The overall aim of our research is to gain novel understanding of regulation of lipid mediators in rheumatoid arthritis (RA) and idiopathic inflammatory myopathies (IIM) to improve treatment of patients.
Microsomal prostaglandin E synthase (mPGES-1) is an attractive alternative target for anti-inflammatory treatment with improved selectivity and safety compared to NSAIDs. Our data suggest that the combination of anti-rheumatic treatments with selective inhibition of mPGES-1 would be beneficial for patients with RA and IIM. To assess the effects of selective inhibition of mPGES-1 on pathogenic mechanisms we perform studies in knock-out mice (mPGES1-/-) and pharmacological modulation of mPGES-1 activity. We aim to compare mechanisms affected by mPGES-1 inhibitors and COX inhibitors in vitro and in vivo models of inflammation and identify novel biomarkers and pathways related to anti-inflammatory or side effects of the drugs.
We have found that both COX- and 5-LO pathways are markedly up-regulated at sites of inflammation in IIM patients. Moreover, our preliminary results suggest a deregulation of lipid metabolism in this disease. We aim to study a role of lipid metabolism/mediators in the pathogenesis of IIM and determine novel biomarkers and potential therapeutic targets.