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Article: B7-H3 and 4-1BBL cooperatively enhance the antitumor response of CD8 T cells in oral cancer

TitleB7-H3 and 4-1BBL cooperatively enhance the antitumor response of CD8 T cells in oral cancer
Authors
Keywords4-1BBL
B7-H3
CD8T cell
Primary oral cancer cell
Issue Date2011
PublisherAmerican Scientific Publishers. The Journal's web site is located at http://www.aspbs.com/science/
Citation
Advanced Science Letters, 2011, v. 4 n. 2, p. 357-362 How to Cite?
Abstract
The aim of this study was to enhance the antitumor immunity of CD8 T cells directed against human oral cancer using B7-H3 and 4-1BBL gene transfer. Recombinant replication-defective adenovirus 5 (Adv) expressing human 4-1BBL, B7-H3 or 4-1BBL/B7-H3 was constructed using the two-plasmid rescue method. Primary human oral cancer cell vaccines (OCV) were prepared by treating cells with 20 μg/ml mitomycin-C after primary human oral cancer cells were infected with Adv transduced with 4-1BBL, B7-H3, 4-1BBL/B7-H3 or control Adv. Then, autologous, purified CD8 T cells were stimulated by coculture with OCV for 4 days. At the end of the culture, CD8 T cell activation was evaluated by ELISA to assay the production of IFNγ and IL-2 in the culture supernatants. Cytotoxic CD8 T cell effector function was analyzed by a 51Chromium (Cr)-release assay, and CD8 T cell proliferation was evaluated by flow cytometry and Cell Counting Kit-8 (CCK-8) assays. Primary human oral cancer cells expressed low levels of B7-H3 and 4-1BBL and weakly stimulated autologous T cells. The primary human oral cancer cell vaccine transduced with the combination of 4-1BBL with B7-H3 retroviruses resulted in significantly enhanced CD8 T cell activation and proliferation. This was associated with increased IFNγ and IL-2 production by CD8 T cells and improved CD8 T cell proliferation. CD8 T cells stimulated with the autologous B7-3/4-1BBL primary human oral cancer cell vaccine efficiently killed the autologous parental B7-H3/4-1BBL primary human oral cancer cells. Strong CD8 T cell activation, proliferation and longer survival time could be obtained by this vaccine. These data provide a mechanism for developing tumor vaccines using modified tumor cells in patients with oral cancer. © 2011 American Scientific Publishers.
Persistent Identifierhttp://hdl.handle.net/10722/134987
ISSN
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China30973339
Guangdong Province Natural Science Foundation104518036002006303
Guangdong Province Science and Technology Agency2010B050100007
foundation of Shenzhen Bureau of Science Technology and InformationJC200903180665A
Funding Information:

This work was supported by the National Natural Science Foundation of China (grant no. 30973339), the Guangdong Province Natural Science Foundation (grant no. 104518036002006303), the Guangdong Province Science and Technology Agency (grant no. 2010B050100007) and the foundation of Shenzhen Bureau of Science Technology and Information (grant no. JC200903180665A).

References

 

Author Affiliations
  1. The University of Hong Kong
  2. Shenzhen-PKU-HKUST Medical Center
  3. Sun Yat-Sen University
  4. Peking University
DC FieldValueLanguage
dc.contributor.authorYu, Sen_HK
dc.contributor.authorTang, Jen_HK
dc.contributor.authorWang, Fen_HK
dc.contributor.authorHuang, Hen_HK
dc.contributor.authorWang, Hen_HK
dc.contributor.authorMa, Pen_HK
dc.contributor.authorZheng, Len_HK
dc.contributor.authorZwahlen, RAen_HK
dc.contributor.authorYang, Hen_HK
dc.date.accessioned2011-07-27T01:25:25Z-
dc.date.available2011-07-27T01:25:25Z-
dc.date.issued2011en_HK
dc.identifier.citationAdvanced Science Letters, 2011, v. 4 n. 2, p. 357-362en_HK
dc.identifier.issn1936-6612en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134987-
dc.description.abstractThe aim of this study was to enhance the antitumor immunity of CD8 T cells directed against human oral cancer using B7-H3 and 4-1BBL gene transfer. Recombinant replication-defective adenovirus 5 (Adv) expressing human 4-1BBL, B7-H3 or 4-1BBL/B7-H3 was constructed using the two-plasmid rescue method. Primary human oral cancer cell vaccines (OCV) were prepared by treating cells with 20 μg/ml mitomycin-C after primary human oral cancer cells were infected with Adv transduced with 4-1BBL, B7-H3, 4-1BBL/B7-H3 or control Adv. Then, autologous, purified CD8 T cells were stimulated by coculture with OCV for 4 days. At the end of the culture, CD8 T cell activation was evaluated by ELISA to assay the production of IFNγ and IL-2 in the culture supernatants. Cytotoxic CD8 T cell effector function was analyzed by a 51Chromium (Cr)-release assay, and CD8 T cell proliferation was evaluated by flow cytometry and Cell Counting Kit-8 (CCK-8) assays. Primary human oral cancer cells expressed low levels of B7-H3 and 4-1BBL and weakly stimulated autologous T cells. The primary human oral cancer cell vaccine transduced with the combination of 4-1BBL with B7-H3 retroviruses resulted in significantly enhanced CD8 T cell activation and proliferation. This was associated with increased IFNγ and IL-2 production by CD8 T cells and improved CD8 T cell proliferation. CD8 T cells stimulated with the autologous B7-3/4-1BBL primary human oral cancer cell vaccine efficiently killed the autologous parental B7-H3/4-1BBL primary human oral cancer cells. Strong CD8 T cell activation, proliferation and longer survival time could be obtained by this vaccine. These data provide a mechanism for developing tumor vaccines using modified tumor cells in patients with oral cancer. © 2011 American Scientific Publishers.en_HK
dc.languageengen_US
dc.publisherAmerican Scientific Publishers. The Journal's web site is located at http://www.aspbs.com/science/en_HK
dc.relation.ispartofAdvanced Science Lettersen_HK
dc.subject4-1BBLen_HK
dc.subjectB7-H3en_HK
dc.subjectCD8T cellen_HK
dc.subjectPrimary oral cancer cellen_HK
dc.titleB7-H3 and 4-1BBL cooperatively enhance the antitumor response of CD8 T cells in oral canceren_HK
dc.typeArticleen_HK
dc.identifier.emailZheng, L:lwzheng@hku.hken_HK
dc.identifier.emailZwahlen, RA:zwahlen@hku.hken_HK
dc.identifier.authorityZheng, L=rp01411en_HK
dc.identifier.authorityZwahlen, RA=rp00055en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1166/asl.2011.1234en_HK
dc.identifier.scopuseid_2-s2.0-79953109589en_HK
dc.identifier.hkuros188024en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79953109589&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue2en_HK
dc.identifier.spage357en_HK
dc.identifier.epage362en_HK
dc.identifier.isiWOS:000291410900013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYu, S=37056474300en_HK
dc.identifier.scopusauthoridTang, J=16239759500en_HK
dc.identifier.scopusauthoridWang, F=37056720800en_HK
dc.identifier.scopusauthoridHuang, H=37055997400en_HK
dc.identifier.scopusauthoridWang, H=37056589500en_HK
dc.identifier.scopusauthoridMa, P=37056073400en_HK
dc.identifier.scopusauthoridZheng, L=11241247300en_HK
dc.identifier.scopusauthoridZwahlen, RA=7004217269en_HK
dc.identifier.scopusauthoridYang, H=37056674200en_HK

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