Pattern of epitopic reactivity of the anti-Hu antibody on HuD with and without paraneoplastic syndrome

Nobuyuki Sodeyama, Kazuyuki Ishida, Kurt A. Jaeckle, Lixin Zhang, Arata Azuma, Masahito Yamada, Hidehiro Mizusawa, Yoshiaki Wada

Research output: Contribution to journalArticle

18 Citations (Scopus)

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 immuno-reacted 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.

Original languageEnglish (US)
Pages (from-to)97-99
Number of pages3
JournalJournal of Neurology Neurosurgery and Psychiatry
Volume66
Issue number1
StatePublished - Jan 1999
Externally publishedYes

Fingerprint

Nervous System Paraneoplastic Syndromes
Paraneoplastic Syndromes
Anti-Idiotypic Antibodies
Amino Acids
Epitopes
Serum
difluprednate
Small Cell Lung Carcinoma
Western Blotting

Keywords

  • Anti-HU antibody
  • Epitope
  • HuD
  • Paraneoplastic syndrome
  • Small cell lung cancer

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Neuroscience(all)
  • Psychiatry and Mental health

Cite this

Sodeyama, N., Ishida, K., Jaeckle, K. A., Zhang, L., Azuma, A., Yamada, M., ... Wada, Y. (1999). Pattern of epitopic reactivity of the anti-Hu antibody on HuD with and without paraneoplastic syndrome. Journal of Neurology Neurosurgery and Psychiatry, 66(1), 97-99.

Pattern of epitopic reactivity of the anti-Hu antibody on HuD with and without paraneoplastic syndrome. / Sodeyama, Nobuyuki; Ishida, Kazuyuki; Jaeckle, Kurt A.; Zhang, Lixin; Azuma, Arata; Yamada, Masahito; Mizusawa, Hidehiro; Wada, Yoshiaki.

In: Journal of Neurology Neurosurgery and Psychiatry, Vol. 66, No. 1, 01.1999, p. 97-99.

Research output: Contribution to journalArticle

Sodeyama, N, Ishida, K, Jaeckle, KA, Zhang, L, Azuma, A, Yamada, M, Mizusawa, H & Wada, Y 1999, 'Pattern of epitopic reactivity of the anti-Hu antibody on HuD with and without paraneoplastic syndrome', Journal of Neurology Neurosurgery and Psychiatry, vol. 66, no. 1, pp. 97-99.
Sodeyama, Nobuyuki ; Ishida, Kazuyuki ; Jaeckle, Kurt A. ; Zhang, Lixin ; Azuma, Arata ; Yamada, Masahito ; Mizusawa, Hidehiro ; Wada, Yoshiaki. / Pattern of epitopic reactivity of the anti-Hu antibody on HuD with and without paraneoplastic syndrome. In: Journal of Neurology Neurosurgery and Psychiatry. 1999 ; Vol. 66, No. 1. pp. 97-99.
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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 immuno-reacted 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.",
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AB - 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 immuno-reacted 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.

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