Purpose of review Recent studies increasingly support a role for autoantibodies in selected chronic pain disorders. This review examines current evidence linking autoantibodies to nociceptive sensitisation and neuroimmune dysfunction across these conditions. Recent findings Experimental and clinical evidence links autoantibodies to altered neuronal excitability, neuroimmune activation, and pain hypersensitivity, particularly within the dorsal root ganglion and spinal sensory circuits. Emerging work further suggests that pathogenicity and treatment responsiveness depend on factors beyond antibody specificity alone, including tissue injury, inflammatory context, and downstream immune signalling mechanisms. Summary Autoimmune pain disorders appear to comprise biologically heterogeneous neuroimmune syndromes in which dorsal root ganglia and anatomically connected sensory pathways emerge as recurring sites of sensitisation. Pathogenicity depends not only on antibody specificity but also on tissue context and downstream neuroimmune mechanisms, supporting the development of more targeted and mechanism-based therapeutic approaches.