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Exciting studies on autoimmune mechanisms of neurologic disorders are leading to the continuous discovery of novel syndromes and autoantibodies of potential clinical utility. Two studies in this issue highlight this discovery process and how findings may be translated into clinical decisions. The first study pertains to the recent discovery of antibodies to cell-adhesion proteins of the nodal and paranodal regions in some patients with chronic inflammatory demyelinating polyneuropathy (CIDP) or Guillain-Barré syndrome. The isotype of these antibodies is usually IgG4, and the target antigens include, among others, contactin-1, neurofascins (NF186 and NF155), and gliomedin, which are important for glial-axonal interactions. Because diseases mediated by antibodies of the IgG4 isotype (such as myasthenia gravis with muscle-specific tyrosine kinase antibodies) often respond to rituximab, Querol et al.1 used a similar approach for 3 patients with severe CIDP and IgG4 antibodies to contactin-1 or NF-155 who were refractory to steroids and IV immunoglobulin (IVIg). Two of the patients had remarkable improvement, and the third showed mild improvement after 10 years of severe disease. As Lancaster and Scherer point out in their editorial, this preliminary observation should encourage determination of whether patients with CIDP who show a poor response to IVIg and steroids have associated IgG4 antibodies. In these cases, B cell–depleting drugs such as rituximab may be effective even after a prolonged course of severe disease.

Name a brain protein, and an autoantibody shall be found!