Impact of FcμR on B-cell receptor induced inflammation in B-cell neoplasia interface patient-derived organoids model
B-cell receptor signalling is a major driver of B-cell leukaemia and lymphomas. Inhibition of Bruton´s tyrosine kinase (BTK), one central molecule of the BCR pathway, results in tremendous response rates in different B-cell neoplasia. Fc receptors (FcRs) contribute to their effector function with their binding to the Fc part of antibodies. The role of FcμR (also called FAIM3 or TOSO) as high affinity Fc receptor for IgM, the primary Ig isotype that already occurs during B-cell development and is a central component of the initial immune response, has barely been explored since its identification in 2009. In particular, its role in leukaemia and lymphoma has been virtually unknown until now. Recently, we identified that FcµR interferes with BCR signalling in malignant B cells resulting in inflammatory signalling, indicating that BCR signalling affects pathways beyond simply survival and migration.