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...
Saved in:
Published in: | Journal of surgical oncology 2009-11, Vol.100 (6), p.500-504 |
---|---|
Main Authors: | , , , , , |
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!
|
Summary: | 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. |
---|---|
ISSN: | 0022-4790 1096-9098 |
DOI: | 10.1002/jso.21376 |