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
LOU BRUNDIN TEAM
Stem cells and inflammation
About
During injuries and inflammation in the central nervous system neural stem/progenitor cells are activated to migrate into the injury. A limited replacement of the injured tissue can be achieved by differentiation of the progenitor cells. The replacement of oligodendrocytes which occurs in the early phases of multiple sclerosis is an example of this mechanism.
Our group works to identify mechanisms important for the regeneration from progenitor cells and how these mechanisms are affected by inflammatory mediators. We have demonstrated that some components in the inflammatory cascade such as nitric oxide can change the fate of the progenitor cells and hampers neurogenesis. We have also demonstrated that progenitor cells carry receptors which on stimulation can cause the release of proinflammatory cytokines from these cells. The aim of our research is to improve the restoration and limit the injury by preservation of restorative mechanisms in the CNS. Our research group consists of neurologists, neurosurgeons and neurobiologists.
Selected publications
Yeung M, Zdunek S, Bergmann O, Bernard S, Salehpour M, Alkass K, et al. Dynamics of oligodendrocyte generation and myelination in the human brain. Cell. 2014 Nov;159(4):766-74.
Pérez Estrada C, Covacu R, Sankavaram S, Svensson M, Brundin L. Oxidative stress increases neurogenesis and oligodendrogenesis in adult neural progenitor cells. Stem Cells Dev. 2014 Oct;23(19):2311-27.
Bergsland M, Covacu R, Perez Estrada C, Svensson M, Brundin L. Nitric oxide-induced neuronal to glial lineage fate-change depends on NRSF/REST function in neural progenitor cells. Stem Cells. 2014 Sep;32(9):2539-49.
Covacu R, Perez Estrada C, Arvidsson L, Svensson M, Brundin L. Change of fate commitment in adult neural progenitor cells subjected to chronic inflammation. J. Neurosci. 2014 Aug;34(35):11571-82.
Confavreux C, O'Connor P, Comi G, Freedman M, Miller A, Olsson T, et al. Oral teriflunomide for patients with relapsing multiple sclerosis (TOWER): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Neurol. 2014 Mar;13(3):247-56.