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Emmy Noether Junior Research Group - Collaboration between autoreactive B cells and Th17 cells during the development and progression of autoimmune inflammatory processes in the CNS

  • Project Leader: Dr. Anneli Peters
  • Affiliation: Institute of Clinical Neuroimmunology
  • Funding: since 2017

Multiple sclerosis (MS) is an autoimmune disease caused by autoreactive T helper cells. Th1 and Th17 cells in particular drive the inflammatory processes in the CNS. For decades, MS research, as well as research in the animal model, the experimental autoimmune encephalomyelitis, has been primarily concerned with autoreactive T cells. The surprising therapeutic success of B-cell depletion therapies in MS patients, however, points to an important role of B cells in pathogenesis. B cells can contribute to inflammatory processes in various ways, namely by producing pathogenic antibodies and/or by presenting antigens and producing cytokines, which in turn promotes the activation and differentiation of autoreactive T cells. Both antibodies and B cells can be detected in the CNS of MS patients - when and why they migrate there and what significance this has for the course of the disease is unclear. Interestingly, B cell infiltrates organized in ectopic lymphoid follicles have been described in some MS patients. In a study of the encephalitogenic properties of different T cell subgroups in the animal model, we discovered similar structures in the CNS of recipients of autoreactive Th17 cells. Since the formation of such ectopic follicles in the CNS was induced exclusively by Th17 cells, but not by other T cell subgroups such as Th1 cells, we suspect that B cells and Th17 cells have a special relationship to each other and co-operatively promote inflammatory processes.

To test this hypothesis, we propose a comprehensive work program that analyzes the interaction of autoreactive B cells and Th17 cells during disease development and progression. For this we will use both transgenic mouse models, which spontaneously develop a B cell-dependent disease, and our adoptive transfer model, with which we can distinguish Th1 and Th17-related effects. The animal models will be analyzed using both traditional immunological methods and intravital microscopy to determine where and when autoreactive B cells and Th17 cells first appear and interact, and whether they activate each other. A detailed phenotypic analysis of B cells from Th17 recipients will provide information on the mechanisms by which Th17 cells promote a pathogenic B cell response. In return, we will also investigate whether B cells can support or inhibit the differentiation of pathogenic Th17 cells through the production of cytokines. The proposed work program will provide important insights into the cellular mechanisms and timing of disease development. This will bring us a step closer to our goal of developing specifically tailored therapeutic approaches for different disease stages.

Source: GEPRIS (Text)