I have an unusual background as I entered medical school on the basis of several years work in hard metal industry. I studied on evenings and succeed to be accepted at medical school at Uppsala University 1977. During the medical courses I became interested in basic research and in particular in immunology and why autoimmune diseases developed. I joined the immunology department led by Hans Wigzell 1981 and completed my PhD 1985. I completed my MD 1987 and was appointed as a docent 1987, everything at Uppsala University. After a short clinical residency career, and some shorter postdoc experiences in US, I was appointed as an associate professor at the Swedish Medical Research Council 1990. I was appointed as a full professor at Lund University 1993 and, happily for me, my entire research group joined in the move to Lund – together we formed the Medical Inflammation Research (MIR) unit at Lund University.
At Lund University we built a platform for genetic analysis of animal models for autoimmune diseases. We were the first to positionally clone genetic polymorphism causing autoimmune diseases, the first discovery was a single nucleotide polymorphism at the Ncf1 gene causing susceptibility to autoimmune diseases in rat models. This polymorphism could later be shown to of major importance also in human autoimmune diseases and contributed to change the view on redox regulation, lack of oxidation could enhance autoimmunity. We have continued to positional clone genes and our current research is based on several of the genes that have been identified, making the focus on relevant targets for regulation of autoimmune diseases more relevant.
In 2008 I was recruited to Karolinska Institute and was located as a professor and head of the section for medial inflammation research. We moved our research group from Lund to Stockholm. On the basis of our basic research we continued to also develop some more applied projects with the aim to enhance the diagnostic tests and developing vaccines to prevent autoimmune diseases. We have continued our genetic research with a strong focus on redox regulation in autoimmunity but we are also looking at the other side of the coin, how redox regulation could help protection against cancer.
To be research leader also requires administrative and economic responsibilities as all research need to be self-financed and be adjusted into a university organisation. Besides this, its and important scientific responsibility, also at the international level, to defend scientific standards. But the beauty of science is still very strongly alive for me, to have the golden opportunity to make new discoveries and discuss research results with my younger coworkers and collegues.
Identification of Clec4b as a novel regulator of bystander activation of auto-reactive T cells and autoimmune disease. Bäckdahl L, Aoun M, Norin U, Holmdahl R PLoS Genet 2020 06;16(6):e1008788
Natural polymorphism of Ym1 regulates pneumonitis through alternative activation of macrophages. Zhu W, Lönnblom E, Förster M, Johannesson M, Tao P, Meng L, et al Sci Adv 2020 Oct;6(43):
Vitamin D3 receptor polymorphisms regulate T cells and T cell-dependent inflammatory diseases. Fernandez Lahore G, Raposo B, Lagerquist M, Ohlsson C, Sabatier P, Xu B, et al Proc Natl Acad Sci U S A 2020 10;117(40):24986-24997
Cartilage-binding antibodies induce pain through immune complex-mediated activation of neurons. Bersellini Farinotti A, Wigerblad G, Nascimento D, Bas DB, Morado Urbina C, Nandakumar KS, et al J. Exp. Med. 2019 Aug;216(8):1904-1924
Cytosolic ROS production by NADPH oxidase 2 regulates muscle glucose uptake during exercise. Henríquez-Olguin C, Knudsen JR, Raun SH, Li Z, Dalbram E, Treebak JT, et al Nat Commun 2019 10;10(1):4623
Structural Basis of Cross-Reactivity of Anti-Citrullinated Protein Antibodies. Ge C, Xu B, Liang B, Lönnblom E, Lundström SL, Zubarev RA, et al 2019 02;71(2):210-221
Mannan-induced Nos2 in macrophages enhances IL-17-driven psoriatic arthritis by innate lymphocytes. Zhong J, Scholz T, Yau ACY, Guerard S, Hüffmeier U, Burkhardt H, et al Sci Adv 2018 05;4(5):eaas9864
T cells specific for post-translational modifications escape intrathymic tolerance induction. Raposo B, Merky P, Lundqvist C, Yamada H, Urbonaviciute V, Niaudet C, et al Nat Commun 2018 01;9(1):353
A single nucleotide polymorphism in the NCF1 gene leading to reduced oxidative burst is associated with systemic lupus erythematosus. Olsson LM, Johansson ÅC, Gullstrand B, Jönsen A, Saevarsdottir S, Rönnblom L, et al Ann. Rheum. Dis. 2017 Sep;76(9):1607-1613