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Interaction of B7-H1 on intrahepatic cholangiocarcinoma cells with PD-1 on tumor-infiltrating T cells as a mechanism of immune evasion
Background and Objectives The B7‐H1/PD‐1 pathway has recently been found to contribute to immune evasion of cancer cells from host immune system. This study aimed to investigate the expression of B7‐H1 and its receptor PD‐1 and to explore their significance in the progression of intraheptic cholangi...
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Published in: | Journal of surgical oncology 2009-11, Vol.100 (6), p.500-504 |
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description | Background and Objectives
The B7‐H1/PD‐1 pathway has recently been found to contribute to immune evasion of cancer cells from host immune system. This study aimed to investigate the expression of B7‐H1 and its receptor PD‐1 and to explore their significance in the progression of intraheptic cholangiocarcinoma (ICC).
Methods
Thirty‐one surgically resected ICC tissues and the corresponding cancer adjacent tissues were enrolled from 2006 to 2007. Immunohistochemical studies were performed with antibody of B7‐H1, PD‐1, CD8, and CD4. Apoptosis status of tumor‐infiltrating lymphocytes (TILs) was detected by TUNEL assay.
Results
Expression of B7‐H1 and PD‐1 was found to be up‐regulated in ICC tissues compared with the cancer adjacent tissues. Tumor‐related B7‐H1 expression was significantly correlated with both tumor differentiation and pTNM stage and was inversely correlated with CD8+ TILs but not CD4+ TILs. TILs in primary carcinoma showed a high level of apoptosis.
Conclusion
B7‐H1/PD‐1 pathway may be linked to malignant potential of ICC and contribute to tumor immune evasion by promoting CD8+ TILs apoptosis. Thus, this pathway may indeed be a potential therapeutic target in the treatment of this disease. J. Surg. Oncol. 2009;100:500–504. © 2009 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/jso.21376 |
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fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_754562399</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67690904</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3936-2ef4f410033c08893d31dc91a36d26f4f64f2e3e706b76f95b9fb851eaba393c3</originalsourceid><addsrcrecordid>eNp9kd9uFCEUxonR2G31whcwXNn0ghaGGVgubdX-SdNqusakN4RhoUsdYAuMtS_gc8t2V3ulCQkk5_d95xw-AN4QvE8wbg5uc9xvCOXsGZgQLBgSWEyfg0mtNajlAm-B7ZxvMcZCsPYl2CKCCU67bgJ-nYZiktLFxQCjhYccnRBY3y6UpBZmqYrTUC_ioMKNi1ol7UL0CmozDBneu7KAnz-gR0kZfUzIBeuGqi0u3MDZhlP1QG_0QgWX_aqR834MBpofKtfWr8ALq4ZsXm_uHfD108fZ0Qk6vzw-PXp_jjQVlKHG2Na2dWdKNZ5OBZ1TMteCKMrmDas11trGUMMx6zmzouuF7acdMapX1UDTHbC79l2meDeaXKR3eTWiCiaOWfKu7VhDhajku_-SjLP6y7it4N4a1CnmnIyVy-S8Sg-SYLmKR9Z45GM8lX27MR17b-ZP5CaPChysgXs3mId_O8mzq8s_lmitcLmYn38VKn2vI1LeyW8XxxJfz86urr_MJKG_AZbdqZc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67690904</pqid></control><display><type>article</type><title>Interaction of B7-H1 on intrahepatic cholangiocarcinoma cells with PD-1 on tumor-infiltrating T cells as a mechanism of immune evasion</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Ye, Yufu ; Zhou, Lin ; Xie, Xiaojun ; Jiang, Guoping ; Xie, Haiyang ; Zheng, Shusen</creator><creatorcontrib>Ye, Yufu ; Zhou, Lin ; Xie, Xiaojun ; Jiang, Guoping ; Xie, Haiyang ; Zheng, Shusen</creatorcontrib><description>Background and Objectives
The B7‐H1/PD‐1 pathway has recently been found to contribute to immune evasion of cancer cells from host immune system. This study aimed to investigate the expression of B7‐H1 and its receptor PD‐1 and to explore their significance in the progression of intraheptic cholangiocarcinoma (ICC).
Methods
Thirty‐one surgically resected ICC tissues and the corresponding cancer adjacent tissues were enrolled from 2006 to 2007. Immunohistochemical studies were performed with antibody of B7‐H1, PD‐1, CD8, and CD4. Apoptosis status of tumor‐infiltrating lymphocytes (TILs) was detected by TUNEL assay.
Results
Expression of B7‐H1 and PD‐1 was found to be up‐regulated in ICC tissues compared with the cancer adjacent tissues. Tumor‐related B7‐H1 expression was significantly correlated with both tumor differentiation and pTNM stage and was inversely correlated with CD8+ TILs but not CD4+ TILs. TILs in primary carcinoma showed a high level of apoptosis.
Conclusion
B7‐H1/PD‐1 pathway may be linked to malignant potential of ICC and contribute to tumor immune evasion by promoting CD8+ TILs apoptosis. Thus, this pathway may indeed be a potential therapeutic target in the treatment of this disease. J. Surg. Oncol. 2009;100:500–504. © 2009 Wiley‐Liss, Inc.</description><identifier>ISSN: 0022-4790</identifier><identifier>EISSN: 1096-9098</identifier><identifier>DOI: 10.1002/jso.21376</identifier><identifier>PMID: 19697355</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Antigens, CD - metabolism ; Apoptosis ; Apoptosis Regulatory Proteins - metabolism ; B7-H1 ; B7-H1 Antigen ; Bile Duct Neoplasms - immunology ; Bile Duct Neoplasms - metabolism ; Bile Duct Neoplasms - pathology ; Bile Ducts, Intrahepatic - metabolism ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; CD8-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - metabolism ; Cholangiocarcinoma - immunology ; Cholangiocarcinoma - metabolism ; Cholangiocarcinoma - pathology ; Female ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; intrahepatic cholangiocarcinoma ; Lymphocyte Count ; Lymphocytes, Tumor-Infiltrating - metabolism ; Lymphocytes, Tumor-Infiltrating - pathology ; Male ; Middle Aged ; PD-1 ; Programmed Cell Death 1 Receptor ; Tumor Escape ; tumor-infiltrating lymphocytes ; Up-Regulation</subject><ispartof>Journal of surgical oncology, 2009-11, Vol.100 (6), p.500-504</ispartof><rights>Copyright © 2009 Wiley‐Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3936-2ef4f410033c08893d31dc91a36d26f4f64f2e3e706b76f95b9fb851eaba393c3</citedby><cites>FETCH-LOGICAL-c3936-2ef4f410033c08893d31dc91a36d26f4f64f2e3e706b76f95b9fb851eaba393c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19697355$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ye, Yufu</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Xie, Xiaojun</creatorcontrib><creatorcontrib>Jiang, Guoping</creatorcontrib><creatorcontrib>Xie, Haiyang</creatorcontrib><creatorcontrib>Zheng, Shusen</creatorcontrib><title>Interaction of B7-H1 on intrahepatic cholangiocarcinoma cells with PD-1 on tumor-infiltrating T cells as a mechanism of immune evasion</title><title>Journal of surgical oncology</title><addtitle>J. Surg. Oncol</addtitle><description>Background and Objectives
The B7‐H1/PD‐1 pathway has recently been found to contribute to immune evasion of cancer cells from host immune system. This study aimed to investigate the expression of B7‐H1 and its receptor PD‐1 and to explore their significance in the progression of intraheptic cholangiocarcinoma (ICC).
Methods
Thirty‐one surgically resected ICC tissues and the corresponding cancer adjacent tissues were enrolled from 2006 to 2007. Immunohistochemical studies were performed with antibody of B7‐H1, PD‐1, CD8, and CD4. Apoptosis status of tumor‐infiltrating lymphocytes (TILs) was detected by TUNEL assay.
Results
Expression of B7‐H1 and PD‐1 was found to be up‐regulated in ICC tissues compared with the cancer adjacent tissues. Tumor‐related B7‐H1 expression was significantly correlated with both tumor differentiation and pTNM stage and was inversely correlated with CD8+ TILs but not CD4+ TILs. TILs in primary carcinoma showed a high level of apoptosis.
Conclusion
B7‐H1/PD‐1 pathway may be linked to malignant potential of ICC and contribute to tumor immune evasion by promoting CD8+ TILs apoptosis. Thus, this pathway may indeed be a potential therapeutic target in the treatment of this disease. J. Surg. Oncol. 2009;100:500–504. © 2009 Wiley‐Liss, Inc.</description><subject>Antigens, CD - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>B7-H1</subject><subject>B7-H1 Antigen</subject><subject>Bile Duct Neoplasms - immunology</subject><subject>Bile Duct Neoplasms - metabolism</subject><subject>Bile Duct Neoplasms - pathology</subject><subject>Bile Ducts, Intrahepatic - metabolism</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>Cholangiocarcinoma - immunology</subject><subject>Cholangiocarcinoma - metabolism</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Female</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>intrahepatic cholangiocarcinoma</subject><subject>Lymphocyte Count</subject><subject>Lymphocytes, Tumor-Infiltrating - metabolism</subject><subject>Lymphocytes, Tumor-Infiltrating - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>PD-1</subject><subject>Programmed Cell Death 1 Receptor</subject><subject>Tumor Escape</subject><subject>tumor-infiltrating lymphocytes</subject><subject>Up-Regulation</subject><issn>0022-4790</issn><issn>1096-9098</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNp9kd9uFCEUxonR2G31whcwXNn0ghaGGVgubdX-SdNqusakN4RhoUsdYAuMtS_gc8t2V3ulCQkk5_d95xw-AN4QvE8wbg5uc9xvCOXsGZgQLBgSWEyfg0mtNajlAm-B7ZxvMcZCsPYl2CKCCU67bgJ-nYZiktLFxQCjhYccnRBY3y6UpBZmqYrTUC_ioMKNi1ol7UL0CmozDBneu7KAnz-gR0kZfUzIBeuGqi0u3MDZhlP1QG_0QgWX_aqR834MBpofKtfWr8ALq4ZsXm_uHfD108fZ0Qk6vzw-PXp_jjQVlKHG2Na2dWdKNZ5OBZ1TMteCKMrmDas11trGUMMx6zmzouuF7acdMapX1UDTHbC79l2meDeaXKR3eTWiCiaOWfKu7VhDhajku_-SjLP6y7it4N4a1CnmnIyVy-S8Sg-SYLmKR9Z45GM8lX27MR17b-ZP5CaPChysgXs3mId_O8mzq8s_lmitcLmYn38VKn2vI1LeyW8XxxJfz86urr_MJKG_AZbdqZc</recordid><startdate>20091101</startdate><enddate>20091101</enddate><creator>Ye, Yufu</creator><creator>Zhou, Lin</creator><creator>Xie, Xiaojun</creator><creator>Jiang, Guoping</creator><creator>Xie, Haiyang</creator><creator>Zheng, Shusen</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20091101</creationdate><title>Interaction of B7-H1 on intrahepatic cholangiocarcinoma cells with PD-1 on tumor-infiltrating T cells as a mechanism of immune evasion</title><author>Ye, Yufu ; Zhou, Lin ; Xie, Xiaojun ; Jiang, Guoping ; Xie, Haiyang ; Zheng, Shusen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3936-2ef4f410033c08893d31dc91a36d26f4f64f2e3e706b76f95b9fb851eaba393c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Antigens, CD - metabolism</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>B7-H1</topic><topic>B7-H1 Antigen</topic><topic>Bile Duct Neoplasms - immunology</topic><topic>Bile Duct Neoplasms - metabolism</topic><topic>Bile Duct Neoplasms - pathology</topic><topic>Bile Ducts, Intrahepatic - metabolism</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - metabolism</topic><topic>Cholangiocarcinoma - immunology</topic><topic>Cholangiocarcinoma - metabolism</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Female</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>intrahepatic cholangiocarcinoma</topic><topic>Lymphocyte Count</topic><topic>Lymphocytes, Tumor-Infiltrating - metabolism</topic><topic>Lymphocytes, Tumor-Infiltrating - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>PD-1</topic><topic>Programmed Cell Death 1 Receptor</topic><topic>Tumor Escape</topic><topic>tumor-infiltrating lymphocytes</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ye, Yufu</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Xie, Xiaojun</creatorcontrib><creatorcontrib>Jiang, Guoping</creatorcontrib><creatorcontrib>Xie, Haiyang</creatorcontrib><creatorcontrib>Zheng, Shusen</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ye, Yufu</au><au>Zhou, Lin</au><au>Xie, Xiaojun</au><au>Jiang, Guoping</au><au>Xie, Haiyang</au><au>Zheng, Shusen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction of B7-H1 on intrahepatic cholangiocarcinoma cells with PD-1 on tumor-infiltrating T cells as a mechanism of immune evasion</atitle><jtitle>Journal of surgical oncology</jtitle><addtitle>J. Surg. Oncol</addtitle><date>2009-11-01</date><risdate>2009</risdate><volume>100</volume><issue>6</issue><spage>500</spage><epage>504</epage><pages>500-504</pages><issn>0022-4790</issn><eissn>1096-9098</eissn><abstract>Background and Objectives
The B7‐H1/PD‐1 pathway has recently been found to contribute to immune evasion of cancer cells from host immune system. This study aimed to investigate the expression of B7‐H1 and its receptor PD‐1 and to explore their significance in the progression of intraheptic cholangiocarcinoma (ICC).
Methods
Thirty‐one surgically resected ICC tissues and the corresponding cancer adjacent tissues were enrolled from 2006 to 2007. Immunohistochemical studies were performed with antibody of B7‐H1, PD‐1, CD8, and CD4. Apoptosis status of tumor‐infiltrating lymphocytes (TILs) was detected by TUNEL assay.
Results
Expression of B7‐H1 and PD‐1 was found to be up‐regulated in ICC tissues compared with the cancer adjacent tissues. Tumor‐related B7‐H1 expression was significantly correlated with both tumor differentiation and pTNM stage and was inversely correlated with CD8+ TILs but not CD4+ TILs. TILs in primary carcinoma showed a high level of apoptosis.
Conclusion
B7‐H1/PD‐1 pathway may be linked to malignant potential of ICC and contribute to tumor immune evasion by promoting CD8+ TILs apoptosis. Thus, this pathway may indeed be a potential therapeutic target in the treatment of this disease. J. Surg. Oncol. 2009;100:500–504. © 2009 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19697355</pmid><doi>10.1002/jso.21376</doi><tpages>5</tpages></addata></record> |
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subjects | Antigens, CD - metabolism Apoptosis Apoptosis Regulatory Proteins - metabolism B7-H1 B7-H1 Antigen Bile Duct Neoplasms - immunology Bile Duct Neoplasms - metabolism Bile Duct Neoplasms - pathology Bile Ducts, Intrahepatic - metabolism CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism CD8-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - metabolism Cholangiocarcinoma - immunology Cholangiocarcinoma - metabolism Cholangiocarcinoma - pathology Female Humans Immunohistochemistry In Situ Nick-End Labeling intrahepatic cholangiocarcinoma Lymphocyte Count Lymphocytes, Tumor-Infiltrating - metabolism Lymphocytes, Tumor-Infiltrating - pathology Male Middle Aged PD-1 Programmed Cell Death 1 Receptor Tumor Escape tumor-infiltrating lymphocytes Up-Regulation |
title | Interaction of B7-H1 on intrahepatic cholangiocarcinoma cells with PD-1 on tumor-infiltrating T cells as a mechanism of immune evasion |
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