Loading…

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...

Full description

Saved in:
Bibliographic Details
Published in:Journal of surgical oncology 2009-11, Vol.100 (6), p.500-504
Main Authors: Ye, Yufu, Zhou, Lin, Xie, Xiaojun, Jiang, Guoping, Xie, Haiyang, Zheng, Shusen
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c3936-2ef4f410033c08893d31dc91a36d26f4f64f2e3e706b76f95b9fb851eaba393c3
cites cdi_FETCH-LOGICAL-c3936-2ef4f410033c08893d31dc91a36d26f4f64f2e3e706b76f95b9fb851eaba393c3
container_end_page 504
container_issue 6
container_start_page 500
container_title Journal of surgical oncology
container_volume 100
creator Ye, Yufu
Zhou, Lin
Xie, Xiaojun
Jiang, Guoping
Xie, Haiyang
Zheng, Shusen
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
format article
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 &amp; 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>
fulltext fulltext
identifier ISSN: 0022-4790
ispartof Journal of surgical oncology, 2009-11, Vol.100 (6), p.500-504
issn 0022-4790
1096-9098
language eng
recordid cdi_proquest_miscellaneous_754562399
source Wiley-Blackwell Read & Publish Collection
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
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T20%3A23%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Interaction%20of%20B7-H1%20on%20intrahepatic%20cholangiocarcinoma%20cells%20with%20PD-1%20on%20tumor-infiltrating%20T%20cells%20as%20a%20mechanism%20of%20immune%20evasion&rft.jtitle=Journal%20of%20surgical%20oncology&rft.au=Ye,%20Yufu&rft.date=2009-11-01&rft.volume=100&rft.issue=6&rft.spage=500&rft.epage=504&rft.pages=500-504&rft.issn=0022-4790&rft.eissn=1096-9098&rft_id=info:doi/10.1002/jso.21376&rft_dat=%3Cproquest_cross%3E67690904%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c3936-2ef4f410033c08893d31dc91a36d26f4f64f2e3e706b76f95b9fb851eaba393c3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=67690904&rft_id=info:pmid/19697355&rfr_iscdi=true