In our next NSI Rising Star Seminar, we will be hosting Søren E. Degn (PhD, Associate Professor, DFF Research Leader and Lundbeckfonden Ascending Investigator) with a talk on “B cells – the bad boys at the back of the bus”. Look forward to seeing you there!
Meeting details:
Speaker: Søren E. Degn
Title: B cells – the bad boys at the back of the bus
Time and date: Thursday, February 27 at 14:00
Meeting link: https://uio.zoom.us/j/67297197985?pwd=bqgeirifg4EMy2Tph8fTcgzqlnWauU.1
Meeting ID: 672 9719 7985
Passcode: 916148
Talk abstract:
B cells are increasingly recognized not simply as precursors of antibody-producing cells, but as central players across a broad range of autoimmune diseases. In recent work, my group demonstrated that B cells can act as primary antigen-presenting cells priming proto-autoreactive T cells and driving epitope spreading in a murine model of systemic lupus erythematosus (Fahlquist-Hagert et al., Nature Communications 2023). Taking this as a starting point, I will touch upon recently published (Fahlquist-Hagert et al., iScience 2024) and unpublished work characterizing the role of T-follicular regulatory cells in curbing autoreactive germinal center responses, including the use of an intravital abdominal imaging window approach for longitudinal studies of immune processes in the spleen (https://doi.org/10.1101/2025.01.06.631523). Finally, I will present ongoing work, in which we have identified a previously unappreciated link between age-associated B cells and CD8 T cell activation and exhaustion.
More information about Søren E. Degn:
Søren completed his BSc (2004) and MSc (2007) in Molecular Biology at Aarhus University. During his MSc, he spent a year at the Departments of Biochemistry and Immunology at the University of Toronto, Canada where he worked with Professor David E. Isenman. Søren then joined the laboratory of Professors Jens Chr. Jensenius and Steffen Thiel, where he completed his PhD in Immunology (2010), on the topic of the lectin pathway of complement. His thesis work included the discovery of a novel regulatory component of this pathway, the protein MAp44 (Degn et al., Journal of Immunology 2009). In the course of his PhD studies, Søren also worked for a year in the laboratory of Professor Michael C. Carroll at the Immune Disease Institute, Harvard Medical School, where he contributed to elucidating how influenza viral antigen is transported and presented in the draining lymph node in a vaccination setting (Gonzalez et al., Nature Immunology 2010). Following award of his PhD degree, Søren continued his work on the lectin pathway of complement as a postdoctoral fellow (2011-2013) with Professors Jens Chr. Jensenius and Steffen Thiel. In a series of papers (Degn et al., Journal of Immunology 2012; Degn et al., Journal of Immunology 2013; Degn et al., PNAS 2014), Søren presented a novel theory for the activation mechanism of the lectin pathway of complement. In 2013, he returned to the laboratory of Professor Michael C. Carroll, now at the Program in Cellular and Molecular Medicine (PCMM) at Boston Children’s Hospital and Harvard Medical School. During his Marie Curie Fellowship at the PCMM, Søren elucidated the clonal evolution of autoreactive germinal centers (Degn et al., Cell 2017), and built his expertise within lymphocyte biology using in vivo models and two-photon microscopy, forming the basis of his return to Aarhus University as a Group Leader and Assistant Professor in 2017. In March 2022, he was promoted to tenured Associate Professor at the Department of Biomedicine. Søren continues to work on autoimmune diseases (van der Poel et al., Cell Reports 2019; Juul-Madsen et al., PNAS 2021; Fahlquist-Hagert et al., Nature Communications 2023), but in recent years his attention has also turned to the molecular mechanism behind antigen-driven activation of the B-cell receptor (Ferapontov, Omer et al, Nature Communications 2023; Degn & Tolar, Nat. Rev. Immunol. 2024).
Google scholar: https://scholar.google.com/citations?user=EyXW-8sAAAAJ&hl=en&oi=ao
Key papers:
1. Antigen presentation by B cells enables epitope spreading across an MHC barrier
2. Antigen footprint governs activation of the B cell receptor