Lymphatic vessel density is associated with CD8<sup>+</sup> T cell infiltration and immunosuppressive factors in human melanoma.
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State: Public
Version: Final published version
License: CC BY-NC-ND 4.0
State: Public
Version: Final published version
License: CC BY-NC-ND 4.0
Serval ID
serval:BIB_AD8EABFF0764
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Lymphatic vessel density is associated with CD8<sup>+</sup> T cell infiltration and immunosuppressive factors in human melanoma.
Journal
Oncoimmunology
ISSN
2162-4011 (Print)
ISSN-L
2162-4011
Publication state
Published
Issued date
2018
Peer-reviewed
Oui
Volume
7
Number
8
Pages
e1462878
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Publication Status: epublish
Abstract
Increased density of tumor-associated lymphatic vessels correlates with poor patient survival in melanoma and other cancers, yet lymphatic drainage is essential for initiating an immune response. Here we asked whether and how lymphatic vessel density (LVD) correlates with immune cell infiltration in primary tumors and lymph nodes (LNs) from patients with cutaneous melanoma. Using immunohistochemistry and quantitative image analysis, we found significant positive correlations between LVD and CD8 <sup>+</sup> T cell infiltration as well as expression of the immunosuppressive molecules inducible nitric oxide synthase (iNOS) and 2,3-dioxygénase (IDO). Interestingly, similar associations were seen in tumor-free LNs adjacent to metastatic ones, indicating loco-regional effects of tumors. Our data suggest that lymphatic vessels play multiple roles at tumor sites and LNs, promoting both T cell infiltration and adaptive immunosuppressive mechanisms. Lymph vessel associated T cell infiltration may increase immunotherapy success rates provided that the treatment overcomes adaptive immune resistance.
Keywords
Immunotherapy, T cell inhibition, T cell promotion, lymphatics, tumor immunology
Pubmed
Web of science
Open Access
Yes
Create date
19/09/2018 14:52
Last modification date
21/11/2022 8:22