Identification of Neuronal Pentraxins as Synaptic Binding Partners of C1q and the Involvement of NP1 in Synaptic Pruning in Adult Mice

Elements of the immune system particularly that innate immunity, play important roles beyond their traditional tasks in host defense, including manifold nervous system. Complement-mediated synaptic pruning is essential developing and healthy functioning brain becomes aberrant neurodegenerative disorders. C1q, component classical complement pathway, plays a central role tagging synapses for elimination; however, underlying molecular mechanisms interaction partners are mostly unknown. Neuronal pentraxins (NPs) involved synapse formation plasticity, moreover, NP1 contributes to cell death neurodegeneration under adverse conditions. Here, we investigated potential between C1q NPs, its microglial phagocytosis adult mice. We verified vitro NPs interact with as well activate Flow cytometry, immunostaining co-immunoprecipitation showed synapse-bound colocalizes interacts NPs. High-resolution confocal microscopy revealed microglia-surrounded C1q-tagged positive. have also observed occurrence C4 suggesting activation pathway cannot be ruled out plasticity animals. In summary, our results indicate regulatory function C1q. Whether this can intensified upon pathological conditions, such Alzheimer’s disease, disclosed.