Avrion Mitchison prize ceremony and Albrecht Hasinger Lecture
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In honor of its Founding Director, Avrion Mitchison, the DRFZ annually awards the Avrion Mitchison Prize to young scientists contributing significantly to understanding and treating rheumatic diseases. Donated by the Ernst Schering Foundation until 2018, the prize is now awarded by the DRFZ. The prize is endowed with 3,000 euros.
The award ceremony took place on 1 December 2020, followed by the Albrecht-Hasinger Lecture. Since 1994, this event has been commemorating Albrecht Hasinger, one of the founding fathers of the DRFZ. The Hasinger Lecture 2020 was given by Professor Christopher Buckley from the University of Birmingham and the Kennedy Institute of Rheumatology, Oxford.
Congratulations to the 2020 Mitchison Prize Awardees
The external jury decided to award the Avrion Mitchison Prize to two candidates: Richard Addo and Lennard Ostendorf. Both gave a presentation about their work.
Bone marrow maintains distinct populations of immunological memory B cells in stromal niches
Memory B cells as one component of immunological memory are important in conferring protective immunity or on the contrary, drive chronic inflammation against repeated antigenic challenges.
Richard Addo: “Our findings address the heterogeneity and maintenance of memory B cells generated during immune responses. We report of exclusive populations of tissue-specific and resident memory B cells in bone marrow and spleen, which differ in their antibody repertoires and gene expression profiles on the levels of single cell and population analyses. In the bone marrow, memory B cells are located in stromal niches. Dissecting the heterogeneity of bone marrow stromal cells, we identified distinct subsets, which express niche supportive factors. This evidence of heterogeneity is valuable in developing therapies aimed at eradicating populations of pathogenic memory B cells which drive local (tissue) and systemic chronic inflammation in rheumatic diseases, by directly targeting these memory B cells and/or indirectly, the stromal cells which organize their survival niches.”
CD38 targeted therapy in Systemic lupus erythematosus
Autoantibodies produced by long-lived plasma cells (LLPC) are drivers of pathogenesis in many autoimmune diseases like systemic lupus erythematosus (SLE). They can survive for decades in dedicated niches and are resistant to conventional immunosuppressive drugs. Previous work demonstrates that targeting of LLPC in SLE can induce long-lasting clinical benefits, but depleting drugs were also associated with considerable toxicity.
Lennard Ostendorf: “Our report describes the treatment of two SLE patients with the anti-CD38 antibody Daratumumab, which lead to sustained clinical responses and LLPC depletion. We are hopeful that targeting CD38 as a well-tolerated modality for the depletion of pathogenic plasma cells can advance the treatment not only of SLE but also of many other antibody-mediated diseases.”
Professor Christopher Buckley
Kennedy Institute of Rheumatology, University of Oxford
Christopher Buckley at the KIR
and University of Birmingham, UK
Christopher Buckley at the University of Birmingham
The implications of the human cell atlas for targeting fibroblasts in immune mediated inflammatory diseases
Besides different immune cells, special cells of the connective tissue, the “fibroblasts”, are important players in rheumatoid arthritis and other chronic inflammatory diseases. Until now, they have been difficult to study and characterize. Hence, there are no approved drugs specifically targeting fibroblasts.
Christopher Buckley investigates the interrelationships between different subsets of fibroblast in the synovium (membrane lining the joint). He observes how selective deletion or modification of these cells impact on the balance between persistent inflammation and tissue damage and the development of arthritis. In his lecture, he will introduce the “Human Cell Atlas”, an international project on constructing a “map” of the different cell types in human organs. The aim is to allow the medical community to move towards an understanding of the cellular basis of diseases and to design better and targeted drugs.