The Role of the CCR5 Receptor in Neuropathic Pain Modulation: Current Insights and Therapeutic Implications

Abstract

Neuropathic pain, a chronic condition arising from injury or dysfunction of the somatosensory nervous system, is characterized by persistent hypersensitivity and spontaneous pain. The chemokine receptor CCR5 (C-C motif chemokine receptor 5) has recently been identified as a critical mediator in neuroinflammation and neuropathic pain signaling pathways. Expressed on immune cells and neurons, CCR5 regulates immune cell recruitment and activation, thereby contributing to neuronal sensitization and maintenance of pain states. This review examines the currently characterized molecular mechanisms through which CCR5 modulates neuropathic pain pathophysiology and assesses the potential of CCR5 antagonists as novel therapeutic agents for the management of chronic neuropathic pain. Understanding the involvement of CCR5 in pain modulation may facilitate the development of targeted treatments with improved efficacy and safety profiles.