Cited by 232Cell death mechanisms and regulationT-cell and B-cell ImmunologyCancer Immunotherapy and Biomarkers

The Fas counterattack: Cancer as a site of immune privilege

O’Connell, Joe, Bennett, Michael W, O’Sullivan, Gerald C, Collins, J.Kevin, Shanahan, Fergus·1999·Immunology Today

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Crossref · 10.1016/s0167-5699(98)01382-6

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120 of 120 references verified0 citation errors · 0 not checkable

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  • Cancer cells directly inhibit the immune system through molecules such as VEGF, prostaglandin E2, TGF-β, and IL-10, which suppress cytotoxic T-cell function.

    “Cancer cells also directly inhibit the immune system through molecules like vascular endothelial growth factor (VEGF), prostaglandin E2, transforming growth factor-β (TGF- β), and interleukin-10 (IL-10), which suppress cytotoxic T-cell function [77,78,80,81,82,83].”

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Authors
O’Connell, J., Bennett, M. W., O’Sullivan, G. C., Collins, J. K., & Shanahan, F.
Affiliations
National University of Ireland (IE)
Corresponding author
  • O’Connell, Joe
  • O’Sullivan, Gerald C
  • Shanahan, Fergus
Venue
Immunology Today
Publisher
Elsevier BV
Published
1999-01
Volume
20
Issue
1
Pages
46-52
ISSN
0167-5699 (ISSN-L)
OpenAlex
W1992386229
Cited by
232
References
120
Citations by year
2024: 3 · 2023: 5 · 2022: 3 · 2021: 1 · 2020: 2 · 2018: 2 · 2017: 3 · 2015: 3 · 2014: 4 · 2013: 1 · 2012: 6
FWCI
2.09
Type
journal article
Language
en
Open access
closed
Locations
  • Immunology Today (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Keywords
Fas, Fas ligand, apoptosis resistance, tumor immunology, immune privilege, tumor immune evasion, cancer immunotherapy
MeSH terms
Immune Tolerance, Immunologic Surveillance, Immunotherapy, Inflammation, Lymphocyte Activation, Membrane Glycoproteins, Neoplasm Proteins, Neoplasms, Polymorphism, Genetic, T-Lymphocytes, Apoptosis, Models, Immunological, fas Receptor, Fas Ligand Protein

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