Pattern of epitopic reactivity of the anti-Hu antibody on HuD with and without paraneoplastic syndrome
- Nobuyuki Sodeyamaa,
- Kazuyuki Ishidaa,
- Kurt A Jaeckleb,
- Lixin Zhangb,
- Arata Azumac,
- Masahito Yamadaa,
- Hidehiro Mizusawaa,
- Yoshiaki Wadaa
- aDepartment of Neurology, Tokyo Medical and Dental University, Tokyo, Japan, bDepartment of Neuro-Oncology, Texas Medical Center, Houston, TX, USA, cFourth Department of Internal Medicine, Nippon Medical School, Tokyo, Japan
- Dr N Sodeyama, Department of Neurology, Tokyo Medical and Dental University, Yushima 1–5–45, Bunkyo-ku, Tokyo 113, Japan. Telephone 0081 3 5803 5234; fax 0081 3 5803 5234; emailn-sodeyama.nuro{at}med.tmd.ac.jp
- Received 20 January 1998
- Revised 17 June 1998
- Accepted 29 June 1998
Abstract
Previous study has shown that the anti-Hu antibody titre of serum samples from patients with paraneoplastic encephalomyelitis/paraneoplastic sensory neuronopathy (PEM/PSN) was significantly higher than that from patients with small cell lung cancer without neurological disturbances (non-PEM/PSN). The aims of this study were (1) to identify the fine epitopes on HuD recognised by the anti-Hu antibody, (2) to determine if the pattern of epitopic reactivity differed between antibodies from patients with and without PEM/PSN, and (3) to determine if the pattern of epitopic reactivity correlated with the clinical features. Recombinant full length HuD and nine deletion fragments were constructed and immunoreacted by western blot analysis with 14 anti-Hu serum samples from eight patients with PEM/PSN and six without PEM/PSN. All anti-Hu serum samples reacted with the deletion fragments containing amino acids (aa) 90–101 or aa 171–206. Some anti-Hu samples reacted with the deletion fragments containing aa 223–234, aa 235–252, or aa 354–373. There was no difference in the pattern of epitopic reactivity between patients with and without PEM/PSN. There was no correlation between the pattern of epitopic reactivity and the clinical features. The anti-Hu antibody titre from patients with PEM/PSN was significantly higher than from patients without PEM/PSN, but there was overlap of their titre concentrations. In conclusion, aa 90–101 and aa 171–206 are the major epitopes with which all anti-Hu serum samples react, and aa 223–234, aa 235–252, and aa 354–373 are the minor epitopes with which only some anti-Hu serum samples react. The analyses suggested that the pattern of epitopic reactivity of the anti-Hu antibody on HuD was not a critical factor for the development or clinical features of PEM/PSN.
