Norwegian Society for Immunology (NSI)

In our next NSI Rising Star Seminar, we will be hosting Mariana Borsa (PhD, Department of Biomedicine, University of Basel) with a talk on “DamAged memories: how autophagy-dependent mitochondrial inheritance shapes T cell diversity”. Look forward to seeing you there!

Meeting details:
Speaker: Mariana Borsa
Title: DamAged memories: how autophagy-dependent mitochondrial inheritance shapes T cell diversity
Time and date: Wednesday, August 13 at 10:00
Meeting link: https://uio.zoom.us/j/61201709553?pwd=O2JaAwQ8427DcwqGCgwwHz36wBxqqa.1

Talk abstract:
T cell immunity is impaired during ageing, particularly in memory responses needed for efficient vaccination. Autophagy and asymmetric cell division (ACD) are cell biological mechanisms key to memory formation, which undergo a decline upon ageing. Thus, we aimed to decipher whether autophagy regulates the early rise of asymmetric T cell fates and investigate whether there is a causal link between ACD and in vivo T cell fate decisions. Proteomic analysis of first-division CD8+ T cells revealed that mitochondrial proteins rely on autophagy for their asymmetric inheritance and that damaged mitochondria are polarized upon first division. Using a novel mouse model to track mitochondrial age, we found that daughter cells inheriting old mitochondria showed reduced quiescence, glycolytic bias, poor survival, and limited memory potential. In contrast, cells devoid of old organelles formed long-lived, functional memory T cells. Multi-omics linked this fate divergence to one-carbon metabolism, modulated by serine availability. Our findings reveal how autophagy and mitochondrial quality imprint early T cell fates—insights with relevance for improving immunity in the context of ageing and regenerative medicine.

More information about Mariana Borsa:
Mariana is an immunologist investigating how organelle inheritance influences immune cell fate. Her previous work has focused on the role of autophagy and asymmetric cell division in the generation of long-lived memory T cells. Originally from Brazil, she earned her PhD in Immunology at ETH Zurich, where she received the ETH Silver Medal for her thesis on T cell fate decisions. To pursue her postdoctoral research at the University of Oxford, she was awarded Sir Henry Wellcome, Marie Skłodowska-Curie, and SNSF fellowships. Her research integrates cell biology, immunology, and metabolism using in vivo models and multi-omics approaches. In September 2025, she will launch her independent lab at the University of Basel, supported by an SNSF Starting Grant.
Google scholar: https://scholar.google.com/citations?user=jcS9CZUAAAAJ&hl=en

Key papers: 
1. Autophagy-regulated mitochondrial inheritance controls early CD8+ T cell fate commitment.
2. Autophagy preserves hematopoietic stem cells by restraining mTORC1-mediated cellular anabolism.
3. Asymmetric cell division shapes naive and virtual memory T-cell immunity during ageing.
4. Modulation of asymmetric cell division as a mechanism to boost CD8 T cell memory.

In our next NSI Rising Star Seminar, we will be hosting Klaus Eyer (PhD, associate professor, Department of Biomedicine, Aarhus University) with a talk on “The Many Functions of individual Immune Cells:  Exploring Polyfunctionality and Polyspecificity on the single-B cell level”. Look forward to seeing you there!

Meeting details:
Speaker: Klaus Eyer
Title: The Many Functions of individual Immune Cells:  Exploring Polyfunctionality and Polyspecificity on the single-B cell level
Time and date: Thursday, June 19 at 14:00
Meeting link: https://uio.zoom.us/j/61981540552

Talk abstract:
Immune responses are driven by various individual cells acting without central coordination. Each cell contributes distinct functions that dynamically adapt, and the collective behavior ultimately shapes the immune outcome. Indeed, single-cell analysis can advance our understanding of these responses with the necessary resolution. While single-cell analysis has advanced significantly in proteomics, genomics and transcriptomics, these approaches only partially reflect actual cellular function and activity. Therefore, our laboratory is working on developing systems to quantify, apply and use individual cellular functions in fundamental questions and clinical applications to unlock their full transformative and translational potential.
During this presentation, we will discuss two very recent, not yet published studies from our laboratory. The first focuses on polyfunctionality of individual B cells, and its temporality – the ability of cells to secrete multiple, distinct proteins either sequentially or simultaneously, and the potential impacts of temporality on function. The second focuses on a new technique that analyzes individual antibodies for their potential to be polyreactive. Indeed, current technologies with single-antibody resolution typically measure binding to only one or a few recombinant antigens, often ignoring specificity and polyreactivity as parameters. We present a method for screening antibody repertoires at single-antibody resolution against a large library of protein variants, using SARS-CoV-2 receptor-binding domain (RBD) mutants to identify the antigenic spectrum of rare, polyreactive antibodies. Using multiplexed antigen sequencing, we performed mutational scanning, enrichment, and escape analysis to map epitopes of the sum and individual polyreactive antibodies within the immunization-generated antibody repertoire.

More information about Klaus Eyer:
Dr. Klaus Eyer has been an associate professor at the Department of Biomedicine at Aarhus University since February 2024. He has a background in pharmaceutical sciences and earned his doctorate in Bioanalytics from ETH Zurich, and his research focuses on functional immune repertoire analysis and single-cell technologies. In the past, Dr. Eyer has held academic positions at ETH Zurich in Switzerland and ESPCI Paris in France and combines different disciplines in his work.
He collaborates locally and internationally on projects related to antibody discovery and immune profiling/characterization, with a focus on their application in neuroinflammation, rare diseases, and personalized medicine. In addition to his research, he is actively involved in teaching, mentoring, and translational activities, including co-founding a biotech start-up, coordinating a doctoral network throughout Europe and contributing to public discussions on science and adaptive immunity following immunization.
Google scholar: https://scholar.google.fr/citations?user=PRtGoGAAAAAJ&hl=en

Key papers: 
1. Single-cell deep phenotyping of cytokine release unmasks stimulation-specific biological signatures and distinct secretion dynamics
2. Single-cell deep phenotyping of IgG-secreting cells for high-resolution immune monitoring

In our next NSI Rising Star Seminar, we will be hosting Tetsuo Hasegawa (PhD, group leader of Molecular Immunity, MRC Laboratory of Molecular Biology, University of Cambridge) with a talk on “3D imaging of the synovium defines an intricate immunological defence system at the blood-joint barrier”. Look forward to seeing you there!

Meeting details:
Speaker: Tetsuo Hasegawa
Title: 3D imaging of the synovium defines an intricate immunological defence system at the blood-joint barrier
Time and date: Thursday, May 15 at 14:00
Meeting link: https://uio.zoom.us/j/64508414976

Talk abstract:
Joint pain or inflammation is a common and early feature of a variety of systemic diseases. These include autoimmune diseases, such as systemic lupus erythematosus (SLE), as well as infection in organs distant to the musculoskeletal system, including enteric or genitourinary infections, which manifest as reactive arthritis. However, why joints are highly responsive to systemic inflammation and where in the joint the inflammation starts are still unknown. We sought to address these questions by developing a whole mount imaging system of the membrane that covers the joint cavity, called synovium, to profile the vascular, neuronal and immune microarchitecture. This revealed that highly permeable capillaries were specifically located at the lining-sublining interface, in the periphery of the synovium, enabling entry of circulating stimuli into the joint. This area of vulnerability was occupied by three subsets of macrophages that demonstrated distinct responses to systemic immune complex challenge and reciprocally interacted with nociceptor neurons, forming a blood-joint barrier (BJB) to defend joint tissue.

More information about Tetsuo Hasegawa:
Dr. Hasegawa is an academic rheumatologist and received his medical degree from Keio University, Japan, in 2011. He went on to complete a Ph.D in the laboratory of Prof. Masaru Ishii at Osaka University, where he identified the pathological osteoclast precursor macrophages and elucidated the mechanism of bone destruction in arthritis. He then began his postdoctoral fellowship in the laboratory of Prof. Menna Clatworthy at University of Cambridge through Human Frontier Science Program long-term fellowship. In 2024, He was awarded the Kennedy Trust Senior Research Fellowship to start his own group in University of Cambridge. His lab is generating a 3D molecular atlas of the membrane in the joint, called synovium, to investigate why joints are responsive to diverse systemic pathologies, how communication between synovial cells and nociceptors influences disease progression, and what mechanisms underlie immune-driven pain in the joints.
Google scholar: https://scholar.google.com/citations?user=R0cIJygAAAAJ&hl=en

Key papers: 
1. Macrophages and nociceptor neurons form a sentinel unit around fenestrated capillaries to defend the synovium from circulating immune challenge
2. Identification of a novel arthritis-associated osteoclast precursor macrophage regulated by FoxM1