Neuropathic Pain Induced by Anti-Caspr2 Autoantibodies: Pathogenesis and Resolution

Autoantibodies targeting Caspr2, a protein associated with voltage-gated potassium channels, have been implicated in neuropathic pain. Despite the presence of these autoantibodies, only a subset of individuals develops chronic pain, and resolution outcomes vary significantly. Prior studies suggest that immune complexes binding to FcγR1 on nociceptive neurons may contribute to neuronal hyperexcitability, yet the underlying mechanisms remain unclear. Understanding these processes is essential for developing targeted treatments for autoantibody-mediated neuropathic pain.

Research Objective

This project will investigate the molecular and cellular mechanisms of neuropathic pain in patients with anti-Caspr2 autoantibodies. We will characterize pain phenotypes, analyze the role of immune complex interactions with nociceptive neurons, and assess transcriptomic changes in dorsal root ganglia neurons. The findings will be expanded to other autoantibody-associated neuropathies to identify common mechanisms and therapeutic targets.

Significance

By elucidating the mechanisms of anti-Caspr2 autoantibody-induced neuropathic pain, the project aims to enable targeted and personalized therapeutic approaches. Identifying relevant pathways may lead to the development of novel strategies that promote pain resolution in patients with autoimmune neuropathies.

Research team NP3

Principal investigators

Apl. Prof. Dr. Kathrin Doppler, MD
Senior Physician of the Department of Neurology
University Hospital Würzburg

Univ.-Prof. Dr. rer. nat. Carmen Villmann
Institute for Clinical Neurobiology
University Hospital Würzburg

Members of the team

Patrik Fischer, PhD Student

Margarita Habib, PhD Student

Luca Buchsteiner, PhD Student

Katharina Fischer, PhD Student

Camille Cauchi, Master Student

Dr. rer. nat. Anna-Lena Wießler, Researcher