B cells are essential for protective immunity but can also contribute to pathological responses, as seen in allergies, autoimmunity, and certain malignancies. This project investigates how antigen recognition by the B-cell receptor triggers intracellular signaling cascades that drive B-cell activation, survival, and differentiation into antibody-secreting plasma cells.

Current B-cell therapies often deplete B cells indiscriminately rather than selectively targeting disease-specific clones. This can compromise immunity, as B cells are critical for producing antibodies in responses to pathogens and vaccines. Advancing therapeutic strategies therefore requires a molecular understanding of the mechanisms that initiate and sustain pathological B-cell responses.

Using an interdisciplinary strategy that combines advanced flow cytometry, precision-engineered antigens, and single-cell analyses, I will define the physicochemical requirements for B-cell activation and investigate how malignant B cells exploit this mechanism to promote their survival and proliferation in an otherwise tightly regulated microenvironment.

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