GENERAL COMMENTARY article

Front. Neurol., 11 March 2019

Sec. Multiple Sclerosis and Neuroimmunology

Volume 10 - 2019 | https://doi.org/10.3389/fneur.2019.00202

Commentary: Detection Methods for Autoantibodies in Suspected Autoimmune Encephalitis

  • Autoimmune Encephalitis and Paraneoplastic Syndromes Clinic, Department of Neurology, Tel-Aviv Medical Center, Tel-Aviv, Israel

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In their paper, Recken and colleagues, review the different autoantibodies, related clinical presentations and cancer associations and detection methods for autoantibodies. The review was comprehensive and nicely described most of the established antibodies. However, when discussing paraneoplastic associated antibodies, the authors failed to mention Purkinje cell antibody type 2 (PCA-2) which is a well-established paraneoplastic antibody (1). PCA-2 has first been described in 2000 by Vernino and Lennon (2) that reported 10 patients with diverse clinical presentations of which 80% had lung cancer. Recently it was discovered that this antibody targets the microtubule associated protein 1B (MAP1B) (3). MAP1B is a part of the microtubule associated protein family that also includes MAP1 (A and B), MAP2 (A and B), and tau protein. These proteins bind and stabilize microtubules. MAP1B expression peaks during early stages of neuronal development and plays an important role in neuronal differentiation, including dendritic spine formation and synaptic maturation (4).

In this recent paper, describing 118 patients, PCA-2 was shown to be as common as anti amphiphysin IgG and more common than ANNA-2 (also known as anti-Ri) and PCA-Tr (also known as delta/notch-like epidermal growth factor-related receptor [DNER]). PCA-2 positivity was associated with cancer in 79% of the patients, with the majority being small cell lung cancer (SCLC) (3).

The clinical presentation among patients varied and included peripheral neuropathy, 53%; cerebellar ataxia, dysmetria, or dysarthria, 38%; and encephalopathy, 27%. Ophthalmologic and spinal involvements were also reported.

MAP1B was shown to present in SCLC as well as in the brain which further support it as a paraneoplastic marker.

The fact that PCA-2 is not yet available in commercial kits, might mistakenly rule out the diagnosis of a paraneoplastic neurological syndrome. This makes including PCA-2 in such a review even more important so it will remain in the differential diagnosis in cases the available commercial kits are negative. In such cases it is important to seek for cancer and if possible use immuno-fluorescence assays available for PCA-2 detection.

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Author contributions

The author confirms being the sole contributor of this work and has approved it for publication.

Conflict of interest

The author published a paper in which MAP1B was described as the antigen of PCA-2. The author is a part of the group that holds a patent on MAP1B as a marker for SCLC and paraneoplastic neurological autoimmunity – patent number 2016-372.

References

  • 1.

    DalmauJRosenfeldMR. Paraneoplastic syndromes of the CNS. Lancet Neurol. (2008) 7:32740. 10.1016/S1474-4422(08)70060-7

  • 2.

    VerninoSLennonVA. New Purkinje cell antibody (PCA-2): marker of lung cancer-related neurological autoimmunity. Ann Neurol. (2000) 47:297305. 10.1002/1531-8249(200003)47:3<297::AID-ANA4>3.0.CO;2-4

  • 3.

    GadothAKryzerTJFryerJMcKeonALennonVAPittockSJ. Microtubule-associated protein 1B: novel paraneoplastic biomarker. Ann Neurol. (2017) 81:26677. 10.1002/ana.24872

  • 4.

    Villarroel-CD Gonzalez-BC. The MAP1B case: an old MAP that is new again. Dev Neurobiol. (2014) 74:95371. 10.1002/dneu.22178

Summary

Keywords

PCA-2, MAP1B, paraneoplastic, autoimmune, small cell lung cancer

Citation

Gadoth A (2019) Commentary: Detection Methods for Autoantibodies in Suspected Autoimmune Encephalitis. Front. Neurol. 10:202. doi: 10.3389/fneur.2019.00202

Received

12 February 2019

Accepted

15 February 2019

Published

11 March 2019

Volume

10 - 2019

Edited by

Thomas G. Forsthuber, University of Texas at San Antonio, United States

Reviewed by

Robert Weissert, University of Regensburg, Germany

Updates

Copyright

*Correspondence: Avi Gadoth

This article was submitted to Multiple Sclerosis and Neuroimmunology, a section of the journal Frontiers in Neurology

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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