Human papillomavirus type 16 E6/E7-specific cytotoxic T lymphocytes for adoptive immunotherapy of HPV-associated malignancies.
Identifieur interne : 001D35 ( PubMed/Curation ); précédent : 001D34; suivant : 001D36Human papillomavirus type 16 E6/E7-specific cytotoxic T lymphocytes for adoptive immunotherapy of HPV-associated malignancies.
Auteurs : Carlos A. Ramos [États-Unis] ; Neeharika Narala ; Gayatri M. Vyas ; Ann M. Leen ; Ulrike Gerdemann ; Erich M. Sturgis ; Matthew L. Anderson ; Barbara Savoldo ; Helen E. Heslop ; Malcolm K. Brenner ; Cliona M. RooneySource :
- Journal of immunotherapy (Hagerstown, Md. : 1997) [ 1537-4513 ] ; 2013.
Descripteurs français
- KwdFr :
- Femelle, Humains, Immunothérapie adoptive, Infections à papillomavirus (), Infections à papillomavirus (immunologie), Lymphocytes T cytotoxiques (immunologie), Papillomavirus humain de type 16 (immunologie), Protéines E7 de papillomavirus (immunologie), Protéines de répression (immunologie), Protéines des oncogènes viraux (immunologie), Tumeurs de l'oropharynx (), Tumeurs de l'oropharynx (immunologie), Tumeurs de l'oropharynx (étiologie), Tumeurs du col de l'utérus (), Tumeurs du col de l'utérus (immunologie), Tumeurs du col de l'utérus (étiologie).
- MESH :
- immunologie : Infections à papillomavirus, Lymphocytes T cytotoxiques, Papillomavirus humain de type 16, Protéines E7 de papillomavirus, Protéines de répression, Protéines des oncogènes viraux, Tumeurs de l'oropharynx, Tumeurs du col de l'utérus.
- étiologie : Tumeurs de l'oropharynx, Tumeurs du col de l'utérus.
- Femelle, Humains, Immunothérapie adoptive, Infections à papillomavirus, Tumeurs de l'oropharynx, Tumeurs du col de l'utérus.
English descriptors
- KwdEn :
- Female, Human papillomavirus 16 (immunology), Humans, Immunotherapy, Adoptive, Oncogene Proteins, Viral (immunology), Oropharyngeal Neoplasms (etiology), Oropharyngeal Neoplasms (immunology), Oropharyngeal Neoplasms (therapy), Papillomavirus E7 Proteins (immunology), Papillomavirus Infections (complications), Papillomavirus Infections (immunology), Papillomavirus Infections (therapy), Repressor Proteins (immunology), T-Lymphocytes, Cytotoxic (immunology), Uterine Cervical Neoplasms (etiology), Uterine Cervical Neoplasms (immunology), Uterine Cervical Neoplasms (therapy).
- MESH :
- chemical , immunology : Oncogene Proteins, Viral, Papillomavirus E7 Proteins, Repressor Proteins.
- complications : Papillomavirus Infections.
- etiology : Oropharyngeal Neoplasms, Uterine Cervical Neoplasms.
- immunology : Human papillomavirus 16, Oropharyngeal Neoplasms, Papillomavirus Infections, T-Lymphocytes, Cytotoxic, Uterine Cervical Neoplasms.
- therapy : Oropharyngeal Neoplasms, Papillomavirus Infections, Uterine Cervical Neoplasms.
- Female, Humans, Immunotherapy, Adoptive.
Abstract
Vaccines prevent human papillomavirus (HPV)-associated cancer but, although these tumors express foreign, viral antigens (E6 and E7 proteins), they have little benefit in established malignancies, likely due to negative environmental cues that block tumor recognition and induce T-cell anergy in vivo. We postulated that we could identify mechanisms by which ex vivo stimulation of T cells could reactivate and expand tumor-directed T-cell lines from HPV cancer patients for subsequent adoptive immunotherapy. A total of 68 patients with HPV-associated cancers were studied. Peripheral blood T cells were stimulated with monocyte-derived dendritic cells loaded with pepmixes [peptide libraries of 15-mers overlapping by 11 amino acids (aa)] spanning E6/E7, in the presence or absence of specific accessory cytokines. The resulting T-cell lines were further expanded with pepmix-loaded activated B-cell blasts. Interferon-γ release and cytotoxic responses to E6/E7 were assessed. We successfully reactivated and expanded (>1200-fold) E6-specific/E7-specific T cells from 8/16 cervical and 33/52 oropharyngeal cancer patients. The presence of the cytokines interleukin (IL)-6, IL-7, IL-12, and IL-15 is critical for this process. These T-cell lines possess the desirable characteristics of polyclonality, multiple T-cell subset representation (including the memory compartment) and a TH1 bias, and may eliminate E6/E7 targets. In conclusion, we have shown it is possible to robustly generate HPV16 E6/E7-directed T-cell lines from patients with HPV16-associated cancers. Because our technique is scalable and good-manufacturing procedures-compliant, these lines could be used for adoptive cellular immunotherapy of patients with HPV16 cancers.
DOI: 10.1097/CJI.0b013e318279652e
PubMed: 23211628
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We postulated that we could identify mechanisms by which ex vivo stimulation of T cells could reactivate and expand tumor-directed T-cell lines from HPV cancer patients for subsequent adoptive immunotherapy. A total of 68 patients with HPV-associated cancers were studied. Peripheral blood T cells were stimulated with monocyte-derived dendritic cells loaded with pepmixes [peptide libraries of 15-mers overlapping by 11 amino acids (aa)] spanning E6/E7, in the presence or absence of specific accessory cytokines. The resulting T-cell lines were further expanded with pepmix-loaded activated B-cell blasts. Interferon-γ release and cytotoxic responses to E6/E7 were assessed. We successfully reactivated and expanded (>1200-fold) E6-specific/E7-specific T cells from 8/16 cervical and 33/52 oropharyngeal cancer patients. The presence of the cytokines interleukin (IL)-6, IL-7, IL-12, and IL-15 is critical for this process. These T-cell lines possess the desirable characteristics of polyclonality, multiple T-cell subset representation (including the memory compartment) and a TH1 bias, and may eliminate E6/E7 targets. In conclusion, we have shown it is possible to robustly generate HPV16 E6/E7-directed T-cell lines from patients with HPV16-associated cancers. Because our technique is scalable and good-manufacturing procedures-compliant, these lines could be used for adoptive cellular immunotherapy of patients with HPV16 cancers.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23211628</PMID><DateCompleted><Year>2013</Year><Month>06</Month><Day>27</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1537-4513</ISSN><JournalIssue CitedMedium="Internet"><Volume>36</Volume><Issue>1</Issue><PubDate><Year>2013</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of immunotherapy (Hagerstown, Md. : 1997)</Title><ISOAbbreviation>J. Immunother.</ISOAbbreviation></Journal><ArticleTitle>Human papillomavirus type 16 E6/E7-specific cytotoxic T lymphocytes for adoptive immunotherapy of HPV-associated malignancies.</ArticleTitle><Pagination><MedlinePgn>66-76</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/CJI.0b013e318279652e</ELocationID><Abstract><AbstractText>Vaccines prevent human papillomavirus (HPV)-associated cancer but, although these tumors express foreign, viral antigens (E6 and E7 proteins), they have little benefit in established malignancies, likely due to negative environmental cues that block tumor recognition and induce T-cell anergy in vivo. We postulated that we could identify mechanisms by which ex vivo stimulation of T cells could reactivate and expand tumor-directed T-cell lines from HPV cancer patients for subsequent adoptive immunotherapy. A total of 68 patients with HPV-associated cancers were studied. Peripheral blood T cells were stimulated with monocyte-derived dendritic cells loaded with pepmixes [peptide libraries of 15-mers overlapping by 11 amino acids (aa)] spanning E6/E7, in the presence or absence of specific accessory cytokines. The resulting T-cell lines were further expanded with pepmix-loaded activated B-cell blasts. Interferon-γ release and cytotoxic responses to E6/E7 were assessed. We successfully reactivated and expanded (>1200-fold) E6-specific/E7-specific T cells from 8/16 cervical and 33/52 oropharyngeal cancer patients. The presence of the cytokines interleukin (IL)-6, IL-7, IL-12, and IL-15 is critical for this process. These T-cell lines possess the desirable characteristics of polyclonality, multiple T-cell subset representation (including the memory compartment) and a TH1 bias, and may eliminate E6/E7 targets. In conclusion, we have shown it is possible to robustly generate HPV16 E6/E7-directed T-cell lines from patients with HPV16-associated cancers. Because our technique is scalable and good-manufacturing procedures-compliant, these lines could be used for adoptive cellular immunotherapy of patients with HPV16 cancers.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ramos</LastName><ForeName>Carlos A</ForeName><Initials>CA</Initials><AffiliationInfo><Affiliation>Center for Cell and Gene Therapy, Baylor College of Medicine, The Methodist Hospital and Texas Children's Hospital, Houston, TX77030, USA. caramos@bcm.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Narala</LastName><ForeName>Neeharika</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Vyas</LastName><ForeName>Gayatri M</ForeName><Initials>GM</Initials></Author><Author ValidYN="Y"><LastName>Leen</LastName><ForeName>Ann M</ForeName><Initials>AM</Initials></Author><Author ValidYN="Y"><LastName>Gerdemann</LastName><ForeName>Ulrike</ForeName><Initials>U</Initials></Author><Author ValidYN="Y"><LastName>Sturgis</LastName><ForeName>Erich M</ForeName><Initials>EM</Initials></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>Matthew L</ForeName><Initials>ML</Initials></Author><Author ValidYN="Y"><LastName>Savoldo</LastName><ForeName>Barbara</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Heslop</LastName><ForeName>Helen E</ForeName><Initials>HE</Initials></Author><Author ValidYN="Y"><LastName>Brenner</LastName><ForeName>Malcolm K</ForeName><Initials>MK</Initials></Author><Author ValidYN="Y"><LastName>Rooney</LastName><ForeName>Cliona M</ForeName><Initials>CM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P20 CA103698</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA023100</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA125123</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 CA097007</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunother</MedlineTA><NlmUniqueID>9706083</NlmUniqueID><ISSNLinking>1524-9557</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C068651">E6 protein, Human papillomavirus type 16</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009856">Oncogene Proteins, Viral</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050725">Papillomavirus E7 Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012097">Repressor Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C059731">oncogene protein E7, Human papillomavirus type 16</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052162" MajorTopicYN="N">Human papillomavirus 16</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016219" MajorTopicYN="Y">Immunotherapy, Adoptive</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009856" MajorTopicYN="N">Oncogene Proteins, Viral</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009959" MajorTopicYN="N">Oropharyngeal Neoplasms</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050725" MajorTopicYN="N">Papillomavirus E7 Proteins</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D030361" MajorTopicYN="N">Papillomavirus Infections</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012097" MajorTopicYN="N">Repressor Proteins</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013602" MajorTopicYN="N">T-Lymphocytes, Cytotoxic</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002583" MajorTopicYN="N">Uterine Cervical Neoplasms</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>12</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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