Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?
Identifieur interne : 000865 ( Istex/Corpus ); précédent : 000864; suivant : 000866Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?
Auteurs : Steven Petratos ; Michael F. GonzalesSource :
- 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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ISTEX:364028DC2528705F5FDEAA0CDC2923FF357D209ELe document en format XML
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Correspondence:
StevenPetratos,
Development and Neurobiology Group, Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050, Australia. Email: <email>petratos@wehi.edu.au</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NEUP.NEUP356.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="4"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="170"></count><count type="wordTotal" number="10996"></count><count type="linksPubMed" number="160"></count><count type="linksCrossRef" number="5"></count></countGroup><titleGroup><title type="main">Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?</title><title type="shortAuthors">S Petratos and MF Gonzales</title><title type="short">Antiglycolipid antibodies and HIV</title></titleGroup><creators><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Steven</givenNames><familyName>Petratos</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>Michael F.</givenNames><familyName>Gonzales</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Development and Neurobiology Group, Walter and Eliza Hall Institute of Medical Research and</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="AU"><unparsedAffiliation>Neuropathology Research Laboratory, Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, Victoria, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">antibodies</keyword><keyword xml:id="k2">galactocerebroside</keyword><keyword xml:id="k3">gangliosides</keyword><keyword xml:id="k4">human immunodeficiency virus</keyword><keyword xml:id="k5">inflammatory demyelinating polyneuropathy</keyword><keyword xml:id="k6">sulfatide</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>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<sub>2</sub> protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM<sub>1</sub>); (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.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Antiglycolipid antibodies and HIV</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?</title></titleInfo><name type="personal"><namePart type="given">Steven</namePart><namePart type="family">Petratos</namePart><affiliation>Development and Neurobiology Group, Walter and Eliza Hall Institute of Medical Research and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael F.</namePart><namePart type="family">Gonzales</namePart><affiliation>Neuropathology Research Laboratory, Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, Victoria, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Science Pty</publisher><place><placeTerm type="text">Melbourne, Australia</placeTerm></place><dateIssued encoding="w3cdtf">2000-12</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">3</extent><extent unit="tables">4</extent><extent unit="formulas">0</extent><extent unit="references">170</extent><extent unit="linksCrossRef">5</extent><extent unit="words">10996</extent></physicalDescription><abstract 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.</abstract><subject lang="en"><genre>keywords</genre><topic>antibodies</topic><topic>galactocerebroside</topic><topic>gangliosides</topic><topic>human immunodeficiency virus</topic><topic>inflammatory demyelinating polyneuropathy</topic><topic>sulfatide</topic></subject><relatedItem type="host"><titleInfo><title>Neuropathology</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0919-6544</identifier><identifier type="eISSN">1440-1789</identifier><identifier type="DOI">10.1111/(ISSN)1440-1789</identifier><identifier type="PublisherID">NEUP</identifier><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>257</start><end>272</end><total>16</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Neurological complications of acquired immune deficiency syndrome, analysis of 50 patients.</title></titleInfo><name type="personal"><namePart type="given">WD</namePart><namePart type="family">Snider</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DM</namePart><namePart type="family">Simpson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Nielson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JWM</namePart><namePart type="family">Gold</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CE</namePart><namePart type="family">Metroka</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JB.</namePart><namePart type="family">Posner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Snider WD, Simpson DM, Nielson S, Gold JWM, Metroka CE & Posner JB. 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