Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?
Identifieur interne : 000845 ( Istex/Curation ); précédent : 000844; suivant : 000846Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?
Auteurs : Steven Petratos ; Michael F. Gonzales [Australie]Source :
- Neuropathology [ 0919-6544 ] ; 2000-12.
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 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) 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.
Url:
DOI: 10.1111/j.1440-1789.2000.00356.x
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Steven Petratos<affiliation><mods:affiliation>Development and Neurobiology Group, Walter and Eliza Hall Institute of Medical Research and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation>Le document en format XML
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Gonzales</name><affiliation wicri:level="1"><mods:affiliation>Neuropathology Research Laboratory, Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, Victoria, Australia</mods:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Neuropathology Research Laboratory, Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, Victoria</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:364028DC2528705F5FDEAA0CDC2923FF357D209E</idno><date when="2000" year="2000">2000</date><idno type="doi">10.1111/j.1440-1789.2000.00356.x</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-L0ZZX345-C/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000865</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000865</idno><idno type="wicri:Area/Istex/Curation">000845</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?</title><author><name sortKey="Petratos, Steven" sort="Petratos, Steven" uniqKey="Petratos S" first="Steven" last="Petratos">Steven Petratos</name><affiliation><mods:affiliation>Development and Neurobiology Group, Walter and Eliza Hall Institute of Medical Research and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Gonzales, Michael F" sort="Gonzales, Michael F" uniqKey="Gonzales M" first="Michael F." last="Gonzales">Michael F. Gonzales</name><affiliation wicri:level="1"><mods:affiliation>Neuropathology Research Laboratory, Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, Victoria, Australia</mods:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Neuropathology Research Laboratory, Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, Victoria</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Neuropathology</title><title level="j" type="alt">NEUROPATHOLOGY</title><idno type="ISSN">0919-6544</idno><idno type="eISSN">1440-1789</idno><imprint><biblScope unit="vol">20</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="257">257</biblScope><biblScope unit="page" to="272">272</biblScope><biblScope unit="page-count">16</biblScope><publisher>Blackwell Science Pty</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2000-12">2000-12</date></imprint><idno type="ISSN">0919-6544</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0919-6544</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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) 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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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