Monospecific high-affinity and complement activating anti-GM1 antibodies are determinants in experimental axonal neuropathy

Notturno, Francesca; Del Boccio, Piero; Luciani, Mirella; Caporale, Christina Michaela; Pieragostino, Damiana; Prencipe, Vincenza; Sacchetta, Paolo; Uncini, Antonino (2010). Monospecific high-affinity and complement activating anti-GM1 antibodies are determinants in experimental axonal neuropathy. Journal of the neurological sciences, 293(1-2), pp. 76-81. Amsterdam: Elsevier 10.1016/j.jns.2010.03.003

Full text not available from this repository. (Request a copy)

It has been difficult to replicate consistently the experimental model of axonal Guillain-Barré syndrome (GBS). We immunized rabbits with two lipo-oligosaccharides (LOS1 and LOS2) derived from the same C. jejuni strain and purified in a slightly different way. LOS1 did not contain proteins whereas several proteins were present in LOS2. In spite of a robust anti-GM1 antibody response in all animals the neuropathy developed only in rabbits immunized with LOS1. To explain this discrepancy we investigated fine specificity, affinity and ability to activate the complement of anti-GM1 antibodies. Only rabbits immunized with LOS1 showed monospecific high-affinity antibodies which activated more effectively the complement. Although it is not well understood how monospecific high-affinity antibodies are induced these are crucial for the induction of experimental axonal neuropathy. Only a strict adherence to the protocols demonstrated to be successful may guarantee the reproducibility and increase the confidence in the animal model as a reliable tool for the study of the human axonal GBS.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurology

UniBE Contributor:

Caporale, Christina Michaela

ISSN:

0022-510X

Publisher:

Elsevier

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:07

Last Modified:

05 Dec 2022 14:00

Publisher DOI:

10.1016/j.jns.2010.03.003

PubMed ID:

20382399

Web of Science ID:

000278652500014

URI:

https://boris.unibe.ch/id/eprint/260 (FactScience: 197148)

Actions (login required)

Edit item Edit item
Provide Feedback