Description:
<jats:title>Abstract</jats:title><jats:p>Chronic inflammatory demyelinating polyneuropathy (<jats:styled-content style="fixed-case">CIDP</jats:styled-content>) is the most common chronic autoimmune neuropathy. While both cell‐mediated and humoral mechanisms contribute to its pathogenesis, the rapid clinical response to plasmapheresis implicates a circulating factor responsible for peripheral nerve injury. We report that treatment‐naïve patients with <jats:styled-content style="fixed-case">CIDP</jats:styled-content> show increased serum and <jats:styled-content style="fixed-case">CSF</jats:styled-content> levels of the anaphylatoxin C5a and the soluble terminal complement complex (<jats:styled-content style="fixed-case">sTCC</jats:styled-content>). Systemic terminal complement activation correlates with clinical disease severity as determined by the Inflammatory Neuropathy Cause and Treatment (<jats:styled-content style="fixed-case">INCAT</jats:styled-content>) disability scale. These data indicate that complement activation contributes to peripheral nerve injury and suggest that complement inhibition should be explored for its potential therapeutic merit in <jats:styled-content style="fixed-case">CIDP</jats:styled-content>.</jats:p>