FoxP3 overexpression and CD1a+ and CD3+ depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection
Identifieur interne : 000F35 ( Istex/Corpus ); précédent : 000F34; suivant : 000F36FoxP3 overexpression and CD1a+ and CD3+ depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection
Auteurs : M. Yaghoobi ; S. Le Gouvello ; N. Aloulou ; C. Duprez- Dutreuil ; F. Walker ; I. SobhaniSource :
- Colorectal Disease [ 1462-8910 ] ; 2011-07.
English descriptors
- Teeft :
- Ain3, Ain3 cancer, Anal, Anal biopsies, Anal canal, Anal cancer, Anal carcinoma, Anal condyloma, Anal mucosa, Anal tissue, Authors colorectal disease, Baseline, Biopsy, Carcinoma, Case group, Cd1a, Cell count, Cell counts, Coloproctology, Colorectal, Control group, Dysplasia, Foxp3, Great britain, Groupe henri chenevier, High prevalence, Hivinfected patients, Human virus, Infection, Infection increases, Invasive carcinoma, Local immunity, Lower grade dysplasia, Multiple regression analysis, Normal biopsies, Odds ratio, Papillomavirus infection, Peripheral blood, Regulatory cells, Risk factors, Roche diagnostics, Study period, Tissue cd1a.
Abstract
Aim We analysed local cellular and humoral immunity factors in the anal mucosa in an attempt to explain how HIV infection increases the risk of anal cancer in HPV‐infected patients. Method HIV‐positive cases and matched HIV‐negative controls with more than one recurrence of condylomas were included in a prospective study following treatment of the initial lesions. Patients were followed every 3 to 6 months for the development of anal intraepithelial neoplasia (AIN3) and cancer for up to 60 months. Tissue CD1a+, CD3+, CD4+, CD8+ cells and mRNAs of selected cytokines and chemokines were quantified and compared in patients with or without AIN3 or cancer using morphometric or immunohistochemistry analysis and qRT‐PCR. Results Sixty‐six individuals (22 patients and 44 controls) were included. In the case group, CD1a+ and CD3+ cell counts were significantly lower in biopsies from AIN3 and cancer specimens compared with those from AIN 1‐2 or normal biopsies (P < 0.0001). A CD1a+ count of < 10/mm was predictive of AIN3 and cancer (Odds ratio = 9.4, 95% CI: 5.4–18.3, P < 0.0001). IL‐8 and IL23 levels were significantly higher in cancer than in non‐cancer tissues regardless of HIV status (P = 0.02). FoxP3 expression was significantly higher in HIV‐infected cases than in controls with AIN3/cancer (P < 0.04). Conclusion Depletion of CD1a+ and CD3+ cells and overexpression of FoxP3 in the anal mucosa appear likely to contribute to the risk of HPV‐related anal cancer in HIV‐infected patients. Furthermore, overexpression of IL‐8 and IL‐23 in the anal mucosa might be responsible for the development of this cancer regardless of HIV status.
Url:
DOI: 10.1111/j.1463-1318.2010.02283.x
Links to Exploration step
ISTEX:F499A4216F28E5D2F099DBF0548D4B6B941EFF9ELe document en format XML
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Le Gouvello</name><affiliation><mods:affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM, Unité 841, Créteil</mods:affiliation></affiliation></author><author><name sortKey="Aloulou, N" sort="Aloulou, N" uniqKey="Aloulou N" first="N." last="Aloulou">N. Aloulou</name><affiliation><mods:affiliation>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</mods:affiliation></affiliation></author><author><name sortKey="Duprez Dutreuil, C" sort="Duprez Dutreuil, C" uniqKey="Duprez Dutreuil C" first="C." last="Duprez- Dutreuil">C. Duprez- Dutreuil</name><affiliation><mods:affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</mods:affiliation></affiliation></author><author><name sortKey="Walker, F" sort="Walker, F" uniqKey="Walker F" first="F." last="Walker">F. 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Yaghoobi</name><affiliation><mods:affiliation>Department of Medicine, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</mods:affiliation></affiliation></author><author><name sortKey="Le Gouvello, S" sort="Le Gouvello, S" uniqKey="Le Gouvello S" first="S." last="Le Gouvello">S. Le Gouvello</name><affiliation><mods:affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM, Unité 841, Créteil</mods:affiliation></affiliation></author><author><name sortKey="Aloulou, N" sort="Aloulou, N" uniqKey="Aloulou N" first="N." last="Aloulou">N. Aloulou</name><affiliation><mods:affiliation>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</mods:affiliation></affiliation></author><author><name sortKey="Duprez Dutreuil, C" sort="Duprez Dutreuil, C" uniqKey="Duprez Dutreuil C" first="C." last="Duprez- Dutreuil">C. Duprez- Dutreuil</name><affiliation><mods:affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</mods:affiliation></affiliation></author><author><name sortKey="Walker, F" sort="Walker, F" uniqKey="Walker F" first="F." last="Walker">F. Walker</name><affiliation><mods:affiliation>AP‐HP, Groupe Bichat Claude Bernard, Service d’anatomie pathologie, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Sobhani, I" sort="Sobhani, I" uniqKey="Sobhani I" first="I." last="Sobhani">I. Sobhani</name><affiliation><mods:affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Colorectal Disease</title><title level="j" type="alt">COLORECTAL DISEASE</title><idno type="ISSN">1462-8910</idno><idno type="eISSN">1463-1318</idno><imprint><biblScope unit="vol">13</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="768">768</biblScope><biblScope unit="page" to="773">773</biblScope><biblScope unit="page-count">6</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-07">2011-07</date></imprint><idno type="ISSN">1462-8910</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1462-8910</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Ain3</term><term>Ain3 cancer</term><term>Anal</term><term>Anal biopsies</term><term>Anal canal</term><term>Anal cancer</term><term>Anal carcinoma</term><term>Anal condyloma</term><term>Anal mucosa</term><term>Anal tissue</term><term>Authors colorectal disease</term><term>Baseline</term><term>Biopsy</term><term>Carcinoma</term><term>Case group</term><term>Cd1a</term><term>Cell count</term><term>Cell counts</term><term>Coloproctology</term><term>Colorectal</term><term>Control group</term><term>Dysplasia</term><term>Foxp3</term><term>Great britain</term><term>Groupe henri chenevier</term><term>High prevalence</term><term>Hivinfected patients</term><term>Human virus</term><term>Infection</term><term>Infection increases</term><term>Invasive carcinoma</term><term>Local immunity</term><term>Lower grade dysplasia</term><term>Multiple regression analysis</term><term>Normal biopsies</term><term>Odds ratio</term><term>Papillomavirus infection</term><term>Peripheral blood</term><term>Regulatory cells</term><term>Risk factors</term><term>Roche diagnostics</term><term>Study period</term><term>Tissue cd1a</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Aim We analysed local cellular and humoral immunity factors in the anal mucosa in an attempt to explain how HIV infection increases the risk of anal cancer in HPV‐infected patients. Method HIV‐positive cases and matched HIV‐negative controls with more than one recurrence of condylomas were included in a prospective study following treatment of the initial lesions. Patients were followed every 3 to 6 months for the development of anal intraepithelial neoplasia (AIN3) and cancer for up to 60 months. Tissue CD1a+, CD3+, CD4+, CD8+ cells and mRNAs of selected cytokines and chemokines were quantified and compared in patients with or without AIN3 or cancer using morphometric or immunohistochemistry analysis and qRT‐PCR. Results Sixty‐six individuals (22 patients and 44 controls) were included. In the case group, CD1a+ and CD3+ cell counts were significantly lower in biopsies from AIN3 and cancer specimens compared with those from AIN 1‐2 or normal biopsies (P < 0.0001). A CD1a+ count of < 10/mm was predictive of AIN3 and cancer (Odds ratio = 9.4, 95% CI: 5.4–18.3, P < 0.0001). IL‐8 and IL23 levels were significantly higher in cancer than in non‐cancer tissues regardless of HIV status (P = 0.02). FoxP3 expression was significantly higher in HIV‐infected cases than in controls with AIN3/cancer (P < 0.04). Conclusion Depletion of CD1a+ and CD3+ cells and overexpression of FoxP3 in the anal mucosa appear likely to contribute to the risk of HPV‐related anal cancer in HIV‐infected patients. Furthermore, overexpression of IL‐8 and IL‐23 in the anal mucosa might be responsible for the development of this cancer regardless of HIV status.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>anal</json:string><json:string>cd1a</json:string><json:string>ain3</json:string><json:string>foxp3</json:string><json:string>anal carcinoma</json:string><json:string>carcinoma</json:string><json:string>colorectal</json:string><json:string>anal mucosa</json:string><json:string>coloproctology</json:string><json:string>case group</json:string><json:string>great britain</json:string><json:string>anal tissue</json:string><json:string>authors colorectal disease</json:string><json:string>biopsy</json:string><json:string>anal condyloma</json:string><json:string>human virus</json:string><json:string>anal biopsies</json:string><json:string>invasive carcinoma</json:string><json:string>baseline</json:string><json:string>dysplasia</json:string><json:string>papillomavirus infection</json:string><json:string>infection increases</json:string><json:string>ain3 cancer</json:string><json:string>anal cancer</json:string><json:string>cell count</json:string><json:string>normal biopsies</json:string><json:string>peripheral blood</json:string><json:string>cell counts</json:string><json:string>high prevalence</json:string><json:string>anal canal</json:string><json:string>odds ratio</json:string><json:string>roche diagnostics</json:string><json:string>groupe henri chenevier</json:string><json:string>study period</json:string><json:string>tissue cd1a</json:string><json:string>lower grade dysplasia</json:string><json:string>multiple regression analysis</json:string><json:string>risk factors</json:string><json:string>control group</json:string><json:string>local immunity</json:string><json:string>regulatory cells</json:string><json:string>hivinfected patients</json:string><json:string>infection</json:string></teeft></keywords><author><json:item><name>M. Yaghoobi</name><affiliations><json:string>Department of Medicine, University of Toronto, Toronto, Ontario, Canada</json:string><json:string>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</json:string></affiliations></json:item><json:item><name>S. Le Gouvello</name><affiliations><json:string>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</json:string><json:string>INSERM, Unité 841, Créteil</json:string></affiliations></json:item><json:item><name>N. Aloulou</name><affiliations><json:string>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</json:string></affiliations></json:item><json:item><name>C. Duprez‐ Dutreuil</name><affiliations><json:string>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</json:string></affiliations></json:item><json:item><name>F. Walker</name><affiliations><json:string>AP‐HP, Groupe Bichat Claude Bernard, Service d’anatomie pathologie, Paris, France</json:string></affiliations></json:item><json:item><name>I. Sobhani</name><affiliations><json:string>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</json:string><json:string>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Anal cancer</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>human papilloma virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>human immunodeficiency virus</value></json:item></subject><articleId><json:string>CODI2283</json:string></articleId><arkIstex>ark:/67375/WNG-DB7P57Z8-M</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Aim We analysed local cellular and humoral immunity factors in the anal mucosa in an attempt to explain how HIV infection increases the risk of anal cancer in HPV‐infected patients. Method HIV‐positive cases and matched HIV‐negative controls with more than one recurrence of condylomas were included in a prospective study following treatment of the initial lesions. Patients were followed every 3 to 6 months for the development of anal intraepithelial neoplasia (AIN3) and cancer for up to 60 months. Tissue CD1a+, CD3+, CD4+, CD8+ cells and mRNAs of selected cytokines and chemokines were quantified and compared in patients with or without AIN3 or cancer using morphometric or immunohistochemistry analysis and qRT‐PCR. Results Sixty‐six individuals (22 patients and 44 controls) were included. In the case group, CD1a+ and CD3+ cell counts were significantly lower in biopsies from AIN3 and cancer specimens compared with those from AIN 1‐2 or normal biopsies (P > 0.0001). A CD1a+ count of > 10/mm was predictive of AIN3 and cancer (Odds ratio = 9.4, 95% CI: 5.4–18.3, P > 0.0001). IL‐8 and IL23 levels were significantly higher in cancer than in non‐cancer tissues regardless of HIV status (P = 0.02). FoxP3 expression was significantly higher in HIV‐infected cases than in controls with AIN3/cancer (P > 0.04). Conclusion Depletion of CD1a+ and CD3+ cells and overexpression of FoxP3 in the anal mucosa appear likely to contribute to the risk of HPV‐related anal cancer in HIV‐infected patients. Furthermore, overexpression of IL‐8 and IL‐23 in the anal mucosa might be responsible for the development of this cancer regardless of HIV status.</abstract><qualityIndicators><score>8.627</score><pdfWordCount>3639</pdfWordCount><pdfCharCount>22967</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><pdfWordsPerPage>607</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>249</abstractWordCount><abstractCharCount>1654</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>FoxP3 overexpression and CD1a+ and CD3+ depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection</title><pmid><json:string>20394639</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Colorectal Disease</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1463-1318</json:string></doi><issn><json:string>1462-8910</json:string></issn><eissn><json:string>1463-1318</json:string></eissn><publisherId><json:string>CODI</json:string></publisherId><volume>13</volume><issue>7</issue><pages><first>768</first><last>773</last><total>6</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Articles</value></json:item><json:item><value>Neoplasia</value></json:item><json:item><value>Original article</value></json:item></subject></host><namedEntities><unitex><date><json:string>2011</json:string><json:string>from June 1993 to June 2004</json:string></date><geogName></geogName><orgName><json:string>National French</json:string><json:string>Roche Diagnostics</json:string><json:string>Immunotech, Marseille, France</json:string><json:string>France Received</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Henri Mondor-Albert</json:string><json:string>S. Le Gouvello</json:string><json:string>Claude Bernard</json:string><json:string>I. Sobhani</json:string><json:string>C. Duprez</json:string><json:string>F. Walker</json:string><json:string>N. Aloulou</json:string></persName><placeName><json:string>Paris</json:string><json:string>USA</json:string><json:string>CA</json:string><json:string>Ireland</json:string><json:string>France</json:string><json:string>Capacity</json:string><json:string>Mountain View</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[4]</json:string><json:string>[10,11]</json:string><json:string>[23]</json:string><json:string>[29]</json:string><json:string>[22]</json:string><json:string>Frisch et al. [5]</json:string><json:string>[8]</json:string><json:string>[28]</json:string><json:string>[25,26]</json:string><json:string>Fox et al.</json:string><json:string>[4,21]</json:string><json:string>M. Yaghoobi et al.</json:string><json:string>[27]</json:string><json:string>[24,25]</json:string><json:string>[20]</json:string><json:string>[3,4]</json:string><json:string>[5]</json:string><json:string>[15]</json:string><json:string>[4,6,9]</json:string><json:string>[6,7]</json:string><json:string>[7]</json:string><json:string>[9]</json:string><json:string>[6,19]</json:string><json:string>[13]</json:string><json:string>[19]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-DB7P57Z8-M</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - surgery</json:string><json:string>2 - gastroenterology & hepatology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - surgery</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Gastroenterology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1111/j.1463-1318.2010.02283.x</json:string></doi><id>F499A4216F28E5D2F099DBF0548D4B6B941EFF9E</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-DB7P57Z8-M/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-DB7P57Z8-M/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/WNG-DB7P57Z8-M/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">FoxP3 overexpression and CD1a+ and CD3+ depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection</title><title level="a" type="short">HIV‐induced changes in FoxP3, CD1a+ and CD3+ in HPV‐related anal carcinoma</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><licence>© 2011 The Authors. Colorectal Disease © 2011 The Association of Coloproctology of Great Britain and Ireland</licence></availability><date type="published" when="2011-07"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">FoxP3 overexpression and CD1a+ and CD3+ depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection</title><title level="a" type="short">HIV‐induced changes in FoxP3, CD1a+ and CD3+ in HPV‐related anal carcinoma</title><author xml:id="author-0000"><persName><forename type="first">M.</forename><surname>Yaghoobi</surname></persName><affiliation><orgName type="division">Department of Medicine</orgName><orgName type="institution">University of Toronto</orgName><address><addrLine>Toronto</addrLine><addrLine>Ontario, Canada</addrLine><country key="CA" xml:lang="en">CANADA</country></address></affiliation><affiliation><address><addrLine>AP‐HP</addrLine><addrLine>Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</addrLine></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">S.</forename><surname>Le Gouvello</surname></persName><affiliation><address><addrLine>AP‐HP</addrLine><addrLine>Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</addrLine></address></affiliation><affiliation><address><addrLine>INSERM</addrLine><addrLine>Unité 841, Créteil</addrLine></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">N.</forename><surname>Aloulou</surname></persName><affiliation><orgName type="institution">Université Paris12</orgName><orgName type="department">Faculté de Médecine‐LIC EA4393</orgName><address><addrLine>Créteil</addrLine></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">C.</forename><surname>Duprez‐ Dutreuil</surname></persName><affiliation><address><addrLine>AP‐HP</addrLine><addrLine>Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</addrLine></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">F.</forename><surname>Walker</surname></persName><affiliation><address><addrLine>AP‐HP</addrLine><addrLine>Groupe Bichat Claude Bernard, Service d’anatomie pathologie, Paris, France</addrLine><country key="FR" xml:lang="en">FRANCE</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">I.</forename><surname>Sobhani</surname></persName><affiliation><address><addrLine>AP‐HP</addrLine><addrLine>Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</addrLine></address></affiliation><affiliation><orgName type="institution">Université Paris12</orgName><orgName type="department">Faculté de Médecine‐LIC EA4393</orgName><address><addrLine>Créteil</addrLine></address></affiliation></author><idno type="istex">F499A4216F28E5D2F099DBF0548D4B6B941EFF9E</idno><idno type="ark">ark:/67375/WNG-DB7P57Z8-M</idno><idno type="DOI">10.1111/j.1463-1318.2010.02283.x</idno><idno type="unit">CODI2283</idno><idno type="toTypesetVersion">file:CODI.CODI2283.pdf</idno></analytic><monogr><title level="j" type="main">Colorectal Disease</title><title level="j" type="alt">COLORECTAL DISEASE</title><idno type="pISSN">1462-8910</idno><idno type="eISSN">1463-1318</idno><idno type="book-DOI">10.1111/(ISSN)1463-1318</idno><idno type="book-part-DOI">10.1111/codi.2011.13.issue-7</idno><idno type="product">CODI</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">13</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="768">768</biblScope><biblScope unit="page" to="773">773</biblScope><biblScope unit="page-count">6</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-07"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p><hi rend="bold">Aim </hi> We analysed local cellular and humoral immunity factors in the anal mucosa in an attempt to explain how HIV infection increases the risk of anal cancer in HPV‐infected patients.</p><p><hi rend="bold">Method </hi> HIV‐positive cases and matched HIV‐negative controls with more than one recurrence of condylomas were included in a prospective study following treatment of the initial lesions. Patients were followed every 3 to 6 months for the development of anal intraepithelial neoplasia (AIN3) and cancer for up to 60 months. Tissue CD1a<hi rend="superscript">+</hi>, CD3<hi rend="superscript">+</hi>, CD4<hi rend="superscript">+</hi>, CD8<hi rend="superscript">+</hi> cells and mRNAs of selected cytokines and chemokines were quantified and compared in patients with or without AIN3 or cancer using morphometric or immunohistochemistry analysis and qRT‐PCR.</p><p><hi rend="bold">Results </hi> Sixty‐six individuals (22 patients and 44 controls) were included. In the case group, CD1a<hi rend="superscript">+</hi> and CD3<hi rend="superscript">+</hi> cell counts were significantly lower in biopsies from AIN3 and cancer specimens compared with those from AIN 1‐2 or normal biopsies (<hi rend="italic">P </hi><<hi rend="italic"> </hi>0.0001). A CD1a<hi rend="superscript">+</hi> count of < 10/mm was predictive of AIN3 and cancer (Odds ratio = 9.4, 95% CI: 5.4–18.3, <hi rend="italic">P </hi><<hi rend="italic"> </hi>0.0001). IL‐8 and IL23 levels were significantly higher in cancer than in non‐cancer tissues regardless of HIV status (<hi rend="italic">P</hi> = 0.02). FoxP3 expression was significantly higher in HIV‐infected cases than in controls with AIN3/cancer (<hi rend="italic">P </hi><<hi rend="italic"> </hi>0.04).</p><p><hi rend="bold">Conclusion </hi> Depletion of CD1a<hi rend="superscript">+</hi> and CD3<hi rend="superscript">+</hi> cells and overexpression of FoxP3 in the anal mucosa appear likely to contribute to the risk of HPV‐related anal cancer in HIV‐infected patients. Furthermore, overexpression of IL‐8 and IL‐23 in the anal mucosa might be responsible for the development of this cancer regardless of HIV status.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">Anal cancer</term><term xml:id="k2">human papilloma virus</term><term xml:id="k3">human immunodeficiency virus</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords><keywords rend="tocHeading2"><term>Neoplasia</term></keywords><keywords rend="articleCategory"><term>Original article</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-DB7P57Z8-M/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1463-1318</doi><issn type="print">1462-8910</issn><issn type="electronic">1463-1318</issn><idGroup><id type="product" value="CODI"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="COLORECTAL DISEASE">Colorectal Disease</title></titleGroup></publicationMeta><publicationMeta level="part" position="07107"><doi origin="wiley">10.1111/codi.2011.13.issue-7</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue" number="7">7</numbering></numberingGroup><coverDate startDate="2011-07">July 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="8" status="forIssue"><doi origin="wiley">10.1111/j.1463-1318.2010.02283.x</doi><idGroup><id type="unit" value="CODI2283"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title><title type="tocHeading2">Neoplasia</title><title type="articleCategory">Original article</title></titleGroup><copyright>© 2011 The Authors. Colorectal Disease © 2011 The Association of Coloproctology of Great Britain and Ireland</copyright><eventGroup><event type="firstOnline" date="2010-04-10"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-04-10"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.5 mode:FullText" date="2011-06-08"></event><event type="publishedOnlineFinalForm" date="2011-06-08"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-16"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="768">768</numbering><numbering type="pageLast" number="773">773</numbering></numberingGroup><correspondenceTo>Iradj Sobhani, Department of Gastroenterology and Hepatology, Henri‐Mondor Hospital, 51 Avenue du Général de Lattre de Tassigny, 94010 Créteil, France.
E‐mail: <email>iradj.sobhani@hmn.aphp.fr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CODI.CODI2283.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 8 October 2009; accepted 22 February 2010; Accepted Article online 10 April 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count></countGroup><titleGroup><title type="main">FoxP3 overexpression and CD1a<sup>+</sup> and CD3<sup>+</sup> depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection</title><title type="shortAuthors"><b><i>M. Yaghoobi</i> et al.</b></title><title type="short">HIV‐induced changes in FoxP3, CD1a<sup>+</sup> and CD3<sup>+</sup> in HPV‐related anal carcinoma</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>M.</givenNames><familyName>Yaghoobi</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a3 #a4"><personName><givenNames>S.</givenNames><familyName>Le Gouvello</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a5"><personName><givenNames>N.</givenNames><familyName>Aloulou</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>C.</givenNames><familyName>Duprez‐ Dutreuil</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a6"><personName><givenNames>F.</givenNames><familyName>Walker</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a2 #a5"><personName><givenNames>I.</givenNames><familyName>Sobhani</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CA"><unparsedAffiliation>Department of Medicine, University of Toronto, Toronto, Ontario, Canada</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>INSERM, Unité 841, Créteil</unparsedAffiliation></affiliation><affiliation xml:id="a5"><unparsedAffiliation>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</unparsedAffiliation></affiliation><affiliation xml:id="a6" countryCode="FR"><unparsedAffiliation>AP‐HP, Groupe Bichat Claude Bernard, Service d’anatomie pathologie, Paris, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Anal cancer</keyword><keyword xml:id="k2">human papilloma virus</keyword><keyword xml:id="k3">human immunodeficiency virus</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p><b>Aim </b> We analysed local cellular and humoral immunity factors in the anal mucosa in an attempt to explain how HIV infection increases the risk of anal cancer in HPV‐infected patients.</p><p><b>Method </b> HIV‐positive cases and matched HIV‐negative controls with more than one recurrence of condylomas were included in a prospective study following treatment of the initial lesions. Patients were followed every 3 to 6 months for the development of anal intraepithelial neoplasia (AIN3) and cancer for up to 60 months. Tissue CD1a<sup>+</sup>, CD3<sup>+</sup>, CD4<sup>+</sup>, CD8<sup>+</sup> cells and mRNAs of selected cytokines and chemokines were quantified and compared in patients with or without AIN3 or cancer using morphometric or immunohistochemistry analysis and qRT‐PCR.</p><p><b>Results </b> Sixty‐six individuals (22 patients and 44 controls) were included. In the case group, CD1a<sup>+</sup> and CD3<sup>+</sup> cell counts were significantly lower in biopsies from AIN3 and cancer specimens compared with those from AIN 1‐2 or normal biopsies (<i>P </i><<i> </i>0.0001). A CD1a<sup>+</sup> count of < 10/mm was predictive of AIN3 and cancer (Odds ratio = 9.4, 95% CI: 5.4–18.3, <i>P </i><<i> </i>0.0001). IL‐8 and IL23 levels were significantly higher in cancer than in non‐cancer tissues regardless of HIV status (<i>P</i> = 0.02). FoxP3 expression was significantly higher in HIV‐infected cases than in controls with AIN3/cancer (<i>P </i><<i> </i>0.04).</p><p><b>Conclusion </b> Depletion of CD1a<sup>+</sup> and CD3<sup>+</sup> cells and overexpression of FoxP3 in the anal mucosa appear likely to contribute to the risk of HPV‐related anal cancer in HIV‐infected patients. Furthermore, overexpression of IL‐8 and IL‐23 in the anal mucosa might be responsible for the development of this cancer regardless of HIV status.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>FoxP3 overexpression and CD1a+ and CD3+ depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>HIV‐induced changes in FoxP3, CD1a+ and CD3+ in HPV‐related anal carcinoma</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>FoxP3 overexpression and CD1a+ and CD3+ depletion in anal tissue as possible mechanisms for increased risk of human papillomavirus‐related anal carcinoma in HIV infection</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Yaghoobi</namePart><affiliation>Department of Medicine, University of Toronto, Toronto, Ontario, Canada</affiliation><affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Le Gouvello</namePart><affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</affiliation><affiliation>INSERM, Unité 841, Créteil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Aloulou</namePart><affiliation>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Duprez‐ Dutreuil</namePart><affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Immunologie biologique, Créteil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Walker</namePart><affiliation>AP‐HP, Groupe Bichat Claude Bernard, Service d’anatomie pathologie, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Sobhani</namePart><affiliation>AP‐HP, Groupe Henri Mondor‐Albert Chenevier, Service d’Hépato‐Gastro‐Entérologie, Créteil</affiliation><affiliation>Université Paris12, Faculté de Médecine‐LIC EA4393, Créteil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-07</dateIssued><edition>Received 8 October 2009; accepted 22 February 2010; Accepted Article online 10 April 2010</edition><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">1</extent><extent unit="tables">3</extent></physicalDescription><abstract lang="en">Aim We analysed local cellular and humoral immunity factors in the anal mucosa in an attempt to explain how HIV infection increases the risk of anal cancer in HPV‐infected patients. Method HIV‐positive cases and matched HIV‐negative controls with more than one recurrence of condylomas were included in a prospective study following treatment of the initial lesions. Patients were followed every 3 to 6 months for the development of anal intraepithelial neoplasia (AIN3) and cancer for up to 60 months. Tissue CD1a+, CD3+, CD4+, CD8+ cells and mRNAs of selected cytokines and chemokines were quantified and compared in patients with or without AIN3 or cancer using morphometric or immunohistochemistry analysis and qRT‐PCR. Results Sixty‐six individuals (22 patients and 44 controls) were included. In the case group, CD1a+ and CD3+ cell counts were significantly lower in biopsies from AIN3 and cancer specimens compared with those from AIN 1‐2 or normal biopsies (P < 0.0001). A CD1a+ count of < 10/mm was predictive of AIN3 and cancer (Odds ratio = 9.4, 95% CI: 5.4–18.3, P < 0.0001). IL‐8 and IL23 levels were significantly higher in cancer than in non‐cancer tissues regardless of HIV status (P = 0.02). FoxP3 expression was significantly higher in HIV‐infected cases than in controls with AIN3/cancer (P < 0.04). Conclusion Depletion of CD1a+ and CD3+ cells and overexpression of FoxP3 in the anal mucosa appear likely to contribute to the risk of HPV‐related anal cancer in HIV‐infected patients. Furthermore, overexpression of IL‐8 and IL‐23 in the anal mucosa might be responsible for the development of this cancer regardless of HIV status.</abstract><subject lang="en"><genre>keywords</genre><topic>Anal cancer</topic><topic>human papilloma virus</topic><topic>human immunodeficiency virus</topic></subject><relatedItem type="host"><titleInfo><title>Colorectal Disease</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><subject><genre>article-category</genre><topic>Original Articles</topic><topic>Neoplasia</topic><topic>Original article</topic></subject><identifier type="ISSN">1462-8910</identifier><identifier type="eISSN">1463-1318</identifier><identifier type="DOI">10.1111/(ISSN)1463-1318</identifier><identifier type="PublisherID">CODI</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>768</start><end>773</end><total>6</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Anal human papillomavirus infection among homosexual and bisexual men: prevalence of type‐specific infection and association with human immunodeficiency virus</title></titleInfo><name type="personal"><namePart type="given">PL</namePart><namePart type="family">Breese</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">FN</namePart><namePart type="family">Judson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KA</namePart><namePart type="family">Penley</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Douglas Jr</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Breese PL, Judson FN, Penley KA, Douglas JM Jr. Anal human papillomavirus infection among homosexual and bisexual men: prevalence of type‐specific infection and association with human immunodeficiency virus. 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