Can antiglycolipid antibodies present in HIV-infected individuals induce immune demyelination?

Steven Petratos, Michael F. Gonzales

Research output: Contribution to journalReview ArticleResearchpeer-review

6 Citations (Scopus)

Abstract

Of the eight clinically defined neuropathies associated with HIV infection, there is compelling evidence that acute and chronic inflammatory demyelinating polyneuropathy (IDPN) have an autoimmune pathogenesis. Many non-HIV infected individuals who suffer from sensory-motor nerve dysfunction have autoimmune indicators. The immunopathogenesis of demyelination must involve neuritogenic components in myelin. The various antigens suspected to play a role in HIV-seronegative IDPN include (i) P2 protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM1); (iv) galactocerebroside (GalC); and (v) glycoproteins or glycolipids with the carbohydrate epitope glucuronyl-3-sulfate. These glycoproteins or glycolipids may be individually targeted, or an immune attack may be raised against a combination of any of these epitopes. The glycolipids, however, especially GalS, have recently evoked much interest as mediators of immune events underlying both non-HIV and HIV-associated demyelinating neuropathies. The present review outlines the recent research findings of antiglycolipid antibodies present in HIV-infected patients with and without peripheral nerve dysfunction, in an attempt to arrive at some consensus as to whether these antibodies may play a role in the immunopathogenesis of HIV-associated inflammatory demyelinating polyneuropathy.

Original languageEnglish
Pages (from-to)257-272
Number of pages16
JournalNeuropathology
Volume20
Issue number4
DOIs
Publication statusPublished - 1 Dec 2000
Externally publishedYes

Keywords

  • Antibodies
  • Galactocerebroside
  • Gangliosides
  • Human immunodeficiency virus
  • Inflammatory demyelinating polyneuropathy
  • Sulfatide

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