Establishment of a fully humanized iPSC-based co-culture model to study interactions between macrophages and sensory neurons.
Discovery that iPSC-derived macrophages (iMacs) undergo specific morphological and secretory changes in direct response to the injury state of sensory neurons.
Evidence that macrophages directly amplify spontaneous firing in damaged sensory neurons, providing a mechanistic link between innate immunity and neuropathic pain.
Identification of neuro-immune signaling pathways as high-priority targets for the development of next-generation non-opioid analgesics.
Background: The Clinical Burden of Neuropathic Pain
