Microglial chimaerism in human xenografts to the rat brain
Identifieur interne : 001878 ( Istex/Corpus ); précédent : 001877; suivant : 001879Microglial chimaerism in human xenografts to the rat brain
Auteurs : Christian Geny ; Souad Naimi-Sadaoui ; Abd El Madjid Belkadi ; Roland Jeny ; Mourad Kammoun ; Marc PeschanskiSource :
- Brain Research Bulletin [ 0361-9230 ] ; 1995.
Abstract
Neural tissue from human fetuses is currently used for intracerebral transplantation to treat patients with Parkinson's disease. The development of the human fetal tissue following grafting has been considered mostly, up to now, from the neuronal point of view in xenografts. Very little is known, in contrast, about nonneuronal, filial, or vascular cells in the grafts. Comparison of the data gathered on the development of grafted human neurons with those obtained in comparable studies using rat transplants has demonstrated species-specific features. We have therefore undertaken a series of studies dealing with non-neuronal cells in human-to-rat transplants to reveal other possible species-specificity of the human tissue. This study has, accordingly, been devoted to the immunohistochemical analysis of microglia of host and donor origins in a human to rat xenograft paradigm allowing clear distinction of the origin of the cells. Human neural tissue was transplanted as a cell suspension into the thalamus of adult rats. Amoeboid human microglia were observed in 1-, 2-, and 3-month-old transplants, but their density, already relatively low at the first stage, decreased further over time. Ramified human microglia were only occasional. In sharp contrast, host rat microglia rapidly invaded the transplant in the absence of any sign of necrosis. The rat cells exhibited first an amoeboid morphology but progressed at the later stages toward a more mature, ramified morphology. These results indicate that donor microglia are quite few in number at first and, at least, do not proliferate actively after transplantation. They seem rather to disappear over time. The parallel migration of a large number of host microglia into the transplant and the apparent maturation of these cells lead to the formation of a cellular chimaera. Extrapolation of these results to clinical neural grafting suggests that most, if not all, microglia in fetal transplants may rapidly be of host origin in patients.
Url:
DOI: 10.1016/0361-9230(95)02004-B
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Département de Biologie, Faculté des Sciences Semlalia-Marrakech, Morocco</mods:affiliation></affiliation></author><author><name sortKey="Belkadi, Abd El Madjid" sort="Belkadi, Abd El Madjid" uniqKey="Belkadi A" first="Abd El Madjid" last="Belkadi">Abd El Madjid Belkadi</name><affiliation><mods:affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Jeny, Roland" sort="Jeny, Roland" uniqKey="Jeny R" first="Roland" last="Jeny">Roland Jeny</name><affiliation><mods:affiliation>Hǒpital Esquirol, 94410 Saint-Maurice, France</mods:affiliation></affiliation></author><author><name sortKey="Kammoun, Mourad" sort="Kammoun, Mourad" uniqKey="Kammoun M" first="Mourad" last="Kammoun">Mourad Kammoun</name><affiliation><mods:affiliation>Hǒpital Esquirol, 94410 Saint-Maurice, France</mods:affiliation></affiliation></author><author><name sortKey="Peschanski, Marc" sort="Peschanski, Marc" uniqKey="Peschanski M" first="Marc" last="Peschanski">Marc Peschanski</name><affiliation><mods:affiliation>To whom requests for reprints should be addressed.</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research Bulletin</title><title level="j" type="abbrev">BRB</title><idno type="ISSN">0361-9230</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995">1995</date><biblScope unit="volume">38</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="383">383</biblScope><biblScope unit="page" to="391">391</biblScope></imprint><idno type="ISSN">0361-9230</idno></series><idno type="istex">D27D781C361F765B4658487FA0CE56C8BB8F70F7</idno><idno type="DOI">10.1016/0361-9230(95)02004-B</idno><idno type="PII">0361-9230(95)02004-B</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0361-9230</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neural tissue from human fetuses is currently used for intracerebral transplantation to treat patients with Parkinson's disease. The development of the human fetal tissue following grafting has been considered mostly, up to now, from the neuronal point of view in xenografts. Very little is known, in contrast, about nonneuronal, filial, or vascular cells in the grafts. Comparison of the data gathered on the development of grafted human neurons with those obtained in comparable studies using rat transplants has demonstrated species-specific features. We have therefore undertaken a series of studies dealing with non-neuronal cells in human-to-rat transplants to reveal other possible species-specificity of the human tissue. This study has, accordingly, been devoted to the immunohistochemical analysis of microglia of host and donor origins in a human to rat xenograft paradigm allowing clear distinction of the origin of the cells. Human neural tissue was transplanted as a cell suspension into the thalamus of adult rats. Amoeboid human microglia were observed in 1-, 2-, and 3-month-old transplants, but their density, already relatively low at the first stage, decreased further over time. Ramified human microglia were only occasional. In sharp contrast, host rat microglia rapidly invaded the transplant in the absence of any sign of necrosis. The rat cells exhibited first an amoeboid morphology but progressed at the later stages toward a more mature, ramified morphology. These results indicate that donor microglia are quite few in number at first and, at least, do not proliferate actively after transplantation. They seem rather to disappear over time. The parallel migration of a large number of host microglia into the transplant and the apparent maturation of these cells lead to the formation of a cellular chimaera. Extrapolation of these results to clinical neural grafting suggests that most, if not all, microglia in fetal transplants may rapidly be of host origin in patients.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Christian Geny</name><affiliations><json:string>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</json:string></affiliations></json:item><json:item><name>Souad Naimi-Sadaoui</name><affiliations><json:string>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</json:string><json:string>Laboratoire de Neurosciences. Département de Biologie, Faculté des Sciences Semlalia-Marrakech, Morocco</json:string></affiliations></json:item><json:item><name>Abd El Madjid Belkadi</name><affiliations><json:string>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</json:string></affiliations></json:item><json:item><name>Roland Jeny</name><affiliations><json:string>Hǒpital Esquirol, 94410 Saint-Maurice, France</json:string></affiliations></json:item><json:item><name>Mourad Kammoun</name><affiliations><json:string>Hǒpital Esquirol, 94410 Saint-Maurice, France</json:string></affiliations></json:item><json:item><name>Marc Peschanski</name><affiliations><json:string>To whom requests for reprints should be addressed.</json:string><json:string>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Human microglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Immunchistochemistry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Brain transplantation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Human fetus</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Neural tissue from human fetuses is currently used for intracerebral transplantation to treat patients with Parkinson's disease. The development of the human fetal tissue following grafting has been considered mostly, up to now, from the neuronal point of view in xenografts. Very little is known, in contrast, about nonneuronal, filial, or vascular cells in the grafts. Comparison of the data gathered on the development of grafted human neurons with those obtained in comparable studies using rat transplants has demonstrated species-specific features. We have therefore undertaken a series of studies dealing with non-neuronal cells in human-to-rat transplants to reveal other possible species-specificity of the human tissue. This study has, accordingly, been devoted to the immunohistochemical analysis of microglia of host and donor origins in a human to rat xenograft paradigm allowing clear distinction of the origin of the cells. Human neural tissue was transplanted as a cell suspension into the thalamus of adult rats. Amoeboid human microglia were observed in 1-, 2-, and 3-month-old transplants, but their density, already relatively low at the first stage, decreased further over time. Ramified human microglia were only occasional. In sharp contrast, host rat microglia rapidly invaded the transplant in the absence of any sign of necrosis. The rat cells exhibited first an amoeboid morphology but progressed at the later stages toward a more mature, ramified morphology. These results indicate that donor microglia are quite few in number at first and, at least, do not proliferate actively after transplantation. They seem rather to disappear over time. The parallel migration of a large number of host microglia into the transplant and the apparent maturation of these cells lead to the formation of a cellular chimaera. Extrapolation of these results to clinical neural grafting suggests that most, if not all, microglia in fetal transplants may rapidly be of host origin in patients.</abstract><qualityIndicators><score>7.445</score><pdfVersion>1.2</pdfVersion><pdfPageSize>620 x 836 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>2003</abstractCharCount><pdfWordCount>4445</pdfWordCount><pdfCharCount>27172</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>305</abstractWordCount></qualityIndicators><title>Microglial chimaerism in human xenografts to the rat brain</title><pii><json:string>0361-9230(95)02004-B</json:string></pii><refBibs><json:item><author><json:item><name>K. Ashwell</name></json:item></author><host><volume>58</volume><pages><last>12</last><first>1</first></pages><author></author><title>Dev. 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Med.</title></host><title>Bilateral fetal mesencephalic grafting in two patients with parkinsonism induced by 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)</title></json:item></refBibs><genre><json:string>research-article</json:string></genre><host><volume>38</volume><pii><json:string>S0361-9230(00)X0012-3</json:string></pii><pages><last>391</last><first>383</first></pages><issn><json:string>0361-9230</json:string></issn><issue>4</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><title>Brain Research Bulletin</title><publicationDate>1995</publicationDate></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1016/0361-9230(95)02004-B</json:string></doi><id>D27D781C361F765B4658487FA0CE56C8BB8F70F7</id><score>0.15726715</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/D27D781C361F765B4658487FA0CE56C8BB8F70F7/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/D27D781C361F765B4658487FA0CE56C8BB8F70F7/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/D27D781C361F765B4658487FA0CE56C8BB8F70F7/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Microglial chimaerism in human xenografts to the rat brain</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1995</date></publicationStmt><notesStmt><note>This article is being published without the benefit of the author's review pf the proofs, which were not available at press time.</note><note type="content">Section title: Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Microglial chimaerism in human xenografts to the rat brain</title><author xml:id="author-1"><persName><forename type="first">Christian</forename><surname>Geny</surname></persName><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Souad</forename><surname>Naimi-Sadaoui</surname></persName><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation><affiliation>Laboratoire de Neurosciences. Département de Biologie, Faculté des Sciences Semlalia-Marrakech, Morocco</affiliation></author><author xml:id="author-3"><persName><forename type="first">Abd El Madjid</forename><surname>Belkadi</surname></persName><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">Roland</forename><surname>Jeny</surname></persName><affiliation>Hǒpital Esquirol, 94410 Saint-Maurice, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">Mourad</forename><surname>Kammoun</surname></persName><affiliation>Hǒpital Esquirol, 94410 Saint-Maurice, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">Marc</forename><surname>Peschanski</surname></persName><affiliation>To whom requests for reprints should be addressed.</affiliation><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation></author></analytic><monogr><title level="j">Brain Research Bulletin</title><title level="j" type="abbrev">BRB</title><idno type="pISSN">0361-9230</idno><idno type="PII">S0361-9230(00)X0012-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">38</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="383">383</biblScope><biblScope unit="page" to="391">391</biblScope></imprint></monogr><idno type="istex">D27D781C361F765B4658487FA0CE56C8BB8F70F7</idno><idno type="DOI">10.1016/0361-9230(95)02004-B</idno><idno type="PII">0361-9230(95)02004-B</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Neural tissue from human fetuses is currently used for intracerebral transplantation to treat patients with Parkinson's disease. The development of the human fetal tissue following grafting has been considered mostly, up to now, from the neuronal point of view in xenografts. Very little is known, in contrast, about nonneuronal, filial, or vascular cells in the grafts. Comparison of the data gathered on the development of grafted human neurons with those obtained in comparable studies using rat transplants has demonstrated species-specific features. We have therefore undertaken a series of studies dealing with non-neuronal cells in human-to-rat transplants to reveal other possible species-specificity of the human tissue. This study has, accordingly, been devoted to the immunohistochemical analysis of microglia of host and donor origins in a human to rat xenograft paradigm allowing clear distinction of the origin of the cells. Human neural tissue was transplanted as a cell suspension into the thalamus of adult rats. Amoeboid human microglia were observed in 1-, 2-, and 3-month-old transplants, but their density, already relatively low at the first stage, decreased further over time. Ramified human microglia were only occasional. In sharp contrast, host rat microglia rapidly invaded the transplant in the absence of any sign of necrosis. The rat cells exhibited first an amoeboid morphology but progressed at the later stages toward a more mature, ramified morphology. These results indicate that donor microglia are quite few in number at first and, at least, do not proliferate actively after transplantation. They seem rather to disappear over time. The parallel migration of a large number of host microglia into the transplant and the apparent maturation of these cells lead to the formation of a cellular chimaera. Extrapolation of these results to clinical neural grafting suggests that most, if not all, microglia in fetal transplants may rapidly be of host origin in patients.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Human microglia</term></item><item><term>Immunchistochemistry</term></item><item><term>Brain transplantation</term></item><item><term>Parkinson's disease</term></item><item><term>Human fetus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-06-03">Modified</change><change when="1995">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/D27D781C361F765B4658487FA0CE56C8BB8F70F7/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>BRB</jid><aid>9502004B</aid><ce:pii>0361-9230(95)02004-B</ce:pii><ce:doi>10.1016/0361-9230(95)02004-B</ce:doi><ce:copyright type="unknown" year="1995"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This article is being published without the benefit of the author's review pf the proofs, which were not available at press time.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>Microglial chimaerism in human xenografts to the rat brain</ce:title><ce:author-group><ce:author><ce:given-name>Christian</ce:given-name><ce:surname>Geny</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Souad</ce:given-name><ce:surname>Naimi-Sadaoui</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF3"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Abd El Madjid</ce:given-name><ce:surname>Belkadi</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Roland</ce:given-name><ce:surname>Jeny</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Mourad</ce:given-name><ce:surname>Kammoun</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Marc</ce:given-name><ce:surname>Peschanski</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>∗</ce:label><ce:textfn>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>†</ce:label><ce:textfn>Hǒpital Esquirol, 94410 Saint-Maurice, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>‡</ce:label><ce:textfn>Laboratoire de Neurosciences. Département de Biologie, Faculté des Sciences Semlalia-Marrakech, Morocco</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>To whom requests for reprints should be addressed.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="24" month="3" year="1995"></ce:date-received><ce:date-revised day="3" month="6" year="1995"></ce:date-revised><ce:date-accepted day="5" month="6" year="1995"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Neural tissue from human fetuses is currently used for intracerebral transplantation to treat patients with Parkinson's disease. The development of the human fetal tissue following grafting has been considered mostly, up to now, from the neuronal point of view in xenografts. Very little is known, in contrast, about nonneuronal, filial, or vascular cells in the grafts. Comparison of the data gathered on the development of grafted human neurons with those obtained in comparable studies using rat transplants has demonstrated species-specific features. We have therefore undertaken a series of studies dealing with non-neuronal cells in human-to-rat transplants to reveal other possible species-specificity of the human tissue. This study has, accordingly, been devoted to the immunohistochemical analysis of microglia of host and donor origins in a human to rat xenograft paradigm allowing clear distinction of the origin of the cells. Human neural tissue was transplanted as a cell suspension into the thalamus of adult rats. Amoeboid human microglia were observed in 1-, 2-, and 3-month-old transplants, but their density, already relatively low at the first stage, decreased further over time. Ramified human microglia were only occasional. In sharp contrast, host rat microglia rapidly invaded the transplant in the absence of any sign of necrosis. The rat cells exhibited first an amoeboid morphology but progressed at the later stages toward a more mature, ramified morphology. These results indicate that donor microglia are quite few in number at first and, at least, do not proliferate actively after transplantation. They seem rather to disappear over time. The parallel migration of a large number of host microglia into the transplant and the apparent maturation of these cells lead to the formation of a cellular chimaera. Extrapolation of these results to clinical neural grafting suggests that most, if not all, microglia in fetal transplants may rapidly be of host origin in patients.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Human microglia</ce:text></ce:keyword><ce:keyword><ce:text>Immunchistochemistry</ce:text></ce:keyword><ce:keyword><ce:text>Brain transplantation</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Human fetus</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Microglial chimaerism in human xenografts to the rat brain</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Microglial chimaerism in human xenografts to the rat brain</title></titleInfo><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Geny</namePart><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Souad</namePart><namePart type="family">Naimi-Sadaoui</namePart><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation><affiliation>Laboratoire de Neurosciences. Département de Biologie, Faculté des Sciences Semlalia-Marrakech, Morocco</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Abd El Madjid</namePart><namePart type="family">Belkadi</namePart><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roland</namePart><namePart type="family">Jeny</namePart><affiliation>Hǒpital Esquirol, 94410 Saint-Maurice, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mourad</namePart><namePart type="family">Kammoun</namePart><affiliation>Hǒpital Esquirol, 94410 Saint-Maurice, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marc</namePart><namePart type="family">Peschanski</namePart><affiliation>To whom requests for reprints should be addressed.</affiliation><affiliation>INSERM U 421, Neuroplasticité et Thérapeutique, Faculté de Médecine, 8 rue général Sarrail, 94010 Créteil Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued><dateModified encoding="w3cdtf">1995-06-03</dateModified><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Neural tissue from human fetuses is currently used for intracerebral transplantation to treat patients with Parkinson's disease. The development of the human fetal tissue following grafting has been considered mostly, up to now, from the neuronal point of view in xenografts. Very little is known, in contrast, about nonneuronal, filial, or vascular cells in the grafts. Comparison of the data gathered on the development of grafted human neurons with those obtained in comparable studies using rat transplants has demonstrated species-specific features. We have therefore undertaken a series of studies dealing with non-neuronal cells in human-to-rat transplants to reveal other possible species-specificity of the human tissue. This study has, accordingly, been devoted to the immunohistochemical analysis of microglia of host and donor origins in a human to rat xenograft paradigm allowing clear distinction of the origin of the cells. Human neural tissue was transplanted as a cell suspension into the thalamus of adult rats. Amoeboid human microglia were observed in 1-, 2-, and 3-month-old transplants, but their density, already relatively low at the first stage, decreased further over time. Ramified human microglia were only occasional. In sharp contrast, host rat microglia rapidly invaded the transplant in the absence of any sign of necrosis. The rat cells exhibited first an amoeboid morphology but progressed at the later stages toward a more mature, ramified morphology. These results indicate that donor microglia are quite few in number at first and, at least, do not proliferate actively after transplantation. They seem rather to disappear over time. The parallel migration of a large number of host microglia into the transplant and the apparent maturation of these cells lead to the formation of a cellular chimaera. Extrapolation of these results to clinical neural grafting suggests that most, if not all, microglia in fetal transplants may rapidly be of host origin in patients.</abstract><note>This article is being published without the benefit of the author's review pf the proofs, which were not available at press time.</note><note type="content">Section title: Article</note><subject><genre>Keywords</genre><topic>Human microglia</topic><topic>Immunchistochemistry</topic><topic>Brain transplantation</topic><topic>Parkinson's disease</topic><topic>Human fetus</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research Bulletin</title></titleInfo><titleInfo type="abbreviated"><title>BRB</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">1995</dateIssued></originInfo><identifier type="ISSN">0361-9230</identifier><identifier type="PII">S0361-9230(00)X0012-3</identifier><part><date>1995</date><detail type="volume"><number>38</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue pages"><start>307</start><end>409</end></extent><extent unit="pages"><start>383</start><end>391</end></extent></part></relatedItem><identifier type="istex">D27D781C361F765B4658487FA0CE56C8BB8F70F7</identifier><identifier type="DOI">10.1016/0361-9230(95)02004-B</identifier><identifier type="PII">0361-9230(95)02004-B</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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