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

Abstract

Neuropathology 2000; 20, 257-272 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 sensorymotor 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) P 2 protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM 1 ); (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 HIVinfected 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.

Presentation of the Same Glycolipid by Different CD1 Molecules

“…Sulfatide is one of the most abundant glycolipids in brain tissue, an important constituent of almost all membranes, and found in the serum at concentrations of 0.5-2.0 M (32). Anti-sulfatide antibodies are present in normal donors and have been observed in patients with peripheral neuropathies associated with IgM paraproteinaemia, or after HIV infection (33)(34)(35). In all of these instances, mainly IgM anti-sulfatide antibodies are found.…”