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.
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Contact: communication@cmm.se
CENTER FOR MOLECULAR MEDICINE
Inflammatory theumatic disease - importance and contribution of B and T cell subjects
Selected publications
VIVIANNE MALMSTRÖM GROUP
Cellular immunology and rheumatic diseases
Inflammatory rheumatic disease – importance and contribution of B and T cell subsets
Many inflammatory rheumatic diseases e.g. RA (rheumatoid arthritis) are characterized by specific sets of autoantibodies and a strong genetic association to distinct HLA class II alleles, which implicate a direct role for B and T cells. Today severe cases are often treated with synthetic and biological therapies targeting different facets of our immune system including B and T cells. Still, there is no cure and we do not understand precisely how T and B cell subsets contribute to disease. We study RA but also SLE, APS (anti-phospholipid syndrome), AAV (ANCA-associated vasculitis) and IIM (myositis).
In the cellular immunology/rheumatology group we aim to
a) Identify disease-specific T and B cells from blood and sites of inflammation in research samples from well-characterized patients.
b) Investigate the functionality of different lymphocyte subsets.
c) Develop assays for immune surveillance, i.e. tracking of antigen- and subset-specific B and T cell in the context of therapeutic intervention and as predictors for clinical outcome.
We study T and B cells in patient samples from the rheumatology clinic, and we collaborate with many research groups and teams including professors Anca Catrina, Elisabet Svenungsson, Iva Gunnarsson and Ingrid Lundberg. Our main method is flow cytometry, and we run and maintain the flow cytometry core at CMM via the work by Annika van Vollenhoven. Moreover, we have an HLA protein lab incorporated into professor Adnane Achours lab at SciLifeLab. Internationally we pursue collaborative efforts within the EU/IMI project RTCure (https://www.rtcure.com).
Selected publications
Carlberg K, Korotkova M, Larsson L, Catrina AI, Ståhl PL*, and Malmström V*. Exploring inflammatory signatures in arthritic joint biopsies with spatial transctipomics. Sci Rep. 2019 Dec 12; 9(1):18975.
Ramsköld D*, Parodis I*, Lakshmikanth T, Chen Y, Zickert A, Sippli N, Mikes J, Amara K, Achour A, Brodin P, Gunnarsson I and Malmström V. B cell alterations during BAFF inhibition with belimumab in SLE patients. eBiomedicine. 2019 Feb; 40:517-27.
Steen J, Forsström B, Sahlström P, Odowd V, Israelsson L, Krishnamurthy A, Badreh S, Mathsson Alm L, Compson J, Ramsköld D, Ndlovu W, Rapecki S, Hansson M, Titcombe PJ, Bang H, Mueller DL, Catrina AI, Grönwall C, Skriner K, Nilsson P, Lightwood D, Klareskog L, Malmström V. Recognition of amino acid motifs, rather than specific proteins, by human plasma cell-derived monoclonal antibodies to posttranslationally modified proteins in rheumatoid arthritis. Arthritis Rheumatol. 2019 Feb; 71(12):196-209.
Titcombe PJ, Wigerblad G, Sippl N, Zhang N, Shmagel AK, Sahlström P, Zhang Y, Barsness LO, Ghodke-Puranik Y, Baharpoor A, Hansson M, Isaelsson L, Niweold TB, Klareskog L, Svensson CI, Amara K, Malmström V* and Mueller DL*. Pathogenic citrulline-multispecific B cell receptor clades in rheumatoid arthritis. Arthritis Rheumatol. 2018 Dec; 70(12):1933-45.
Pieper J, Dubnovitsky A, James E, Gerstner C, Rieck M, Gebe JA, Achour A, Buckner JH and Malmström V Memory T cells specific to citrullinated α-enolase are enriched in the rheumatic joint. J Autoimmunity. 2018 Aug; 92:47-56.
Chemin K, Ramsköld D, Diaz-Gallo L_M, Herrath J, Tandre K, Rönnblom L, Catrina IA and Malmström V. EOMES-positive CD4+ T cells are increased in PTPN22 (1858T) risk allele carriers. Eur J Immunol. 2018 Apr; 48(4):655-669.
Malmström V, Catrina AI, Klareskog L. The immunopathogenesis of seropositive rheumatoid arthritis: from triggering to targeting. Nat Rev Immunol. 2017 Jan;17(1):60-75.
Gerstner C, Dubnovitsky A, Sandin C, Kozhukh G, Uchtenhagen H, James EA, Rönnelid J, Ytterberg AJ, Pieper J, Reed E, Tandre C, Rieck M, Zubarev RA, Rönnblom L, Sandalova T, Buckner JH, Achour A, Malmström V. Functional and Structural Characterization of a Novel HLA-DRB1*04:01-Restricted α-Enolase T Cell Epitope in Rheumatoid Arthritis. Front Immunol. 2016 Nov 14;7:494.
Pandya JM, Venalis P, Al-Khalili L, Shahadat Hossain M, Stache V, Lundberg IE, Malmström V, Fasth AE. CD4+ and CD8+ CD28(null) T Cells Are Cytotoxic to Autologous Muscle Cells in Patients With Polymyositis. Arthritis Rheumatol. 2016 Aug;68(8):2016-26.
Pandya JM, Loell I, Hossain MS, Zong M, Alexanderson H, Raghavan S, Lundberg IE, Malmström V. Effects of conventional immunosuppressive treatment on CD244+ (CD28null) and FOXP3+ T cells in the inflamed muscle of patients with polymyositis and dermatomyositis. Arthritis Res Ther. 2016 Apr 1;18:80.
Herrath J, Chemin K, Albrecht I, Catrina AI and Malmström V. Surface expression of CD39 identifies an enriched Treg subset in the rheumatic joint, which is impaired in suppressing IL-17A secretion. Eur J Immunol. 2014 Oct; 44:2979-89.
James E*, Rieck M*, Pieper J, Gebe JA, Yue BB, Tatum M, Peda M, Sandin C, Klareskog L, Malmström V and Buckner JH. Citrulline-specific Th1 cells are increased in rheumatoid arthritis and their frequency is influenced by disease duration and therapy. Arthritis Rheum. 2014 Jul; 66:1712-22
Fasth AER, Björkström NK, Anthoni M, Malmberg K-J and Malmström V. Activating NK-cell receptors co-stimulate CD4(+)CD28(-) T cells in patients with rheumatoid arthritis. Eur J Immunol. 2010 Feb; 40:378-87.
Vallerskog T, Gunnarsson I, Widhe M, Risselada A, Klareskog L, van Vollenhoven R, Malmström V and Trollmo C. Treatment with rituximab affects both the cellular and the humoral arm of the immune system in patients with SLE. Clin Immunol. 2007 Jan; 122:62-74.