Neuropathic pain (NP) is an intractable pain caused by a lesion or disease of the somatosensory nervous system. Some causes of NP are well-known, but in many cases it is difficult to identify the cause of NP. Therefore, it is challenging to treat it appropriately. Recently, the interaction between NP and autoantibodies has attracted increasing attention in the field of autoimmune neurology. Autoantibodies against contactin-associated protein-like 2 (Caspr2) and Plexin D1, which expressed by dorsal root ganglion (DRG) neurons, were reported in a fraction of patients with NP. NP in patients with these autoantibodies was reduced by immunotherapy and treatments such as plasma exchange. Moreover, the passive transfer of purified IgG from these patients to mice induced pain hypersensitivity via the activation of DRG neurons. These findings support the idea that these autoantibodies are pathogenic for NP. Hence, detection of pathogenic autoantibodies in NP could be a useful guide for selecting patients with NP eligible for immunotherapy, for whom no treatment options are available except for analgesics, which have only limited efficacy. In this symposium, I describe the concept of autoantibody-related NP and latest research inspired by autoantibody-related NP.