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
ENIKÖ SONKOLY
Exploring the role and therapeutic potential of non-coding RNAs in chronic skin inflammation
About
Skin is our largest organ, representing an interface between the organism and the environment. The uppermost part of the skin, the epidermis is a continuously renewing tissue governed by a tightly regulated differentiation program. Being much more than just a physical barrier, the epidermis is a complex immunological barrier that can recognize and respond to external stimuli including pathogens.
Psoriasis and atopic dermatitis are the most common chronic inflammatory skin diseases, and they have a significant impact on the quality of life of the affected patients. In these chronic inflammatory skin diseases, activation of the immune system in interaction with keratinocytes, the main cell type in the epidermis, sustains chronic inflammation.
Non-coding RNAs, constituting a large part of transcriptional output in our cells, have important regulatory functions in the cells. Both short (e.g. miRNAs) and long (long non-coding RNAs, lncRNAs) have emerged as important gene regulators in health and disease.
Our research
Our research aims to explore how non-coding RNAs contribute to chronic inflammatory skin diseases, and their potential as biomarkers and therapy targets. For this, we use patient samples, cell culture, 3D epidermal models and animal models of skin inflammation. We have identified several miRNAs that regulate crucial cellular functions in psoriasis and their modulation affects skin inflammation in preclinical models.
Exploring the function of non-coding RNAs in skin diseases also sheds light on their functions in the complex regulatory networks that ensure proper epidermal differentiation and immune responses but prevent excessive inflammation in normal skin.
Grant support
National Psoriasis Foundation (USA), Discovery Grant, 75000 USD, 2019-2021
ALF Medicine Project Grant, 1.500.000 SEK, 2019-2021
KID Grant, 50% support for a PhD student 2021- (to be recruited)
Swedish Research Council, Half-time Position in Clinical Research Environment, 1 850 000 SEK/ year 2016-2018
ALF Medicine project grant, 929 000 SEK, 2016-2017
KID grant for Ankit Srivastava (2014-2018) and Lorenzo Pasquali (2016-2020)
Åke Wibergs Foundation, 300 000 SEK, 2015
Inflammation Europe ASPIRE 2014 research award (Pfizer), 515 221 SEK, 2015
The Swedish Skin Foundation, 800 000 SEK, 2015-2016
Psoriasisförbundet, 150 000 kr, 2015-2016
KI Research Foundation, 27 600 SEK, 2014-2015
Psoriasisförbundet, 150 000 SEK, 2013
National Psoriasis Foundation (USA), 200 000 USD, 2012-2014
Selected publications
Pasquali L, Svedbom A, Srivastava A, Rosén E, Lindqvist U, Ståhle M, Pivarcsi A, Sonkoly E. Circulating microRNAs in extracellular vesicles as potential biomarkers for psoriatic arthritis in patients with psoriasis. J Eur Acad Dermatol 2020 34;6 1248-1256
Srivastava A, Meisgen F, Pasquali L, Munkhammar S, Xia P, Stahle M, Landen NX, Pivarcsi A, Sonkoly E. Next-Generation Sequencing Identifies the Keratinocyte-Specific miRNA Signature of Psoriasis. J Invest Dermatol 2019 139;12 2547-2550.e12
Pasquali L, Srivastava A, Meisgen F, Das Mahapatra K, Xia P, Xu Landén N, Pivarcsi A, Sonkoly E. The Keratinocyte Transcriptome in Psoriasis: Pathways Related to Immune Responses, Cell Cycle and Keratinization. Acta derm vener 2019 99;2 196-205
Srivastava A, Ståhle M, Pivarcsi A, Sonkoly E. Tofacitinib Represses the Janus Kinase-Signal Transducer and Activators of Transcription Signalling Pathway in Keratinocytes. Acta derm vener 2018 98;8 772-775
Srivastava A, Nikamo P, Lohcharoenkal W, Li D, Meisgen F, Xu Landén N, Ståhle M, Pivarcsi A, Sonkoly E. MicroRNA-146a suppresses IL-17-mediated skin inflammation and is genetically associated with psoriasis. J Allergy Clin Immunol. 2017 Feb;139(2):550-561.
Meisgen F, Xu Landén N, Wang A, Réthi B, Bouez C, Zuccolo M, Gueniche A, Ståhle M, Sonkoly E, Breton L, Pivarcsi A. MiR-146a negatively regulates TLR2-induced inflammatory responses in keratinocytes. J Invest Dermatol. 2014 Jul;134(7):1931-1940.
Meisgen F, Xu Landén N, Bouez C, Zuccolo M, Gueniche A, Ståhle M, Sonkoly E, Breton L, Pivarcsi A. Activation of Toll-like receptors alters the microRNA expression profile of keratinocytes. Exp Dermatol. 2014 Apr;23(4):281-3.
Pivarcsi A, Meisgen F, Xu N, Ståhle M, Sonkoly E. Changes in the level of serum microRNAs in psoriasis patients after anti-tumor necrosis factor-α therapy. Br J Dermatol. 2013 Sep;169(3):563-70.
Xu N, Meisgen F, Butler LM, Han G, Wang XJ, Söderberg-Nauclér C, Ståhle M, Pivarcsi A, Sonkoly E. MicroRNA-31 is overexpressed in psoriasis and modulates inflammatory cytokine and chemokine production in keratinocytes via targeting STK40. J Immunol. 2013 Jan 15;190(2):678-88.
Meisgen F, Xu N, Wei T, Janson PC, Obad S, Broom O, Nagy N, Kauppinen S, Kemény L, Ståhle M, Pivarcsi A, Sonkoly E. MiR-21 is up-regulated in psoriasis and suppresses T cell apoptosis. Exp Dermatol. 2012 Apr;21(4):312-4.
Wei T, Orfanidis K, Xu N, Janson P, Ståhle M, Pivarcsi A and Sonkoly E. The expression of microRNA-203 during human skin morphogenesis. Exp. Dermatol. 2010 Sep;19(9):854-6
Sonkoly E, Janson P, Majuri M, Savinko T, Fyhrquist N, Xu N, Wei T, Stenvang J, Kauppinen S, Alenius H, Lauerma A, Homey B, Winqvist O, Ståhle M, Pivarcsi A. MiR-155 is overexpressed in atopic dermatitis and modulates T cell proliferative responses by targeting CTLA-4. J All Clin Immunol. 2010 Sep;126(3):581-9.e1-20.
Sonkoly E, Wei T, Pavez Loriè E, Suzuki H, Kato M, Törmä H, Ståhle M, Pivarcsi A. Protein kinase C-dependent upregulation of miR-203 induces the differentiation of human keratinocytes. J Invest Dermatol. 2010 Jan;130(1):124-34.
E Sonkoly, T Wei, PC Janson, A Saaf, L Lundeberg, M Tengvall-Linder, G Norstedt, H Alenius, B Homey, A Scheynius, M Stahle, A Pivarcsi. MicroRNAs: novel regulators involved in the pathogenesis of Psoriasis? PLoS ONE. 2007 Jul 11;2(7):e610.