T cell exclusion, immune privilege, and the tumor microenvironment

By J. Joyce, D. Fearon. Science, 2015

2,161 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/284fddf670bbf37bded4c9a3a6f0956c37c2e71d

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In Immunology

In Oncology

Citations in the corpus

Crosstalk between cancer-associated fibroblasts and immune cells in the tumor microenvironment: new findings and future perspectives (2021, background): “The CAFremodeled ECM protein network serves as a physical barrier for immune cells, especially T lymphocytes, thus inhibiting their recruitment into cancer sites and subsequently reducing their opportunities to participate in the immune response in the TME [279, 280].”
Cytotoxic CD8+ T cells in cancer and cancer immunotherapy (2020, background): “Furthermore, within the bulk of a tumour, CD8 T cells need to actively navigate and seek out cancer cells—direct contact between T cells and cancer cells is decisive in determining the outcomes.(81) Inadequate CD8 T-cell navigation within a tumour represents a serious resistance mechanism: the amoun”
Simultaneous enumeration of cancer and immune cell types from bulk tumor gene expression data (2017, background): “Tumors form complex microenvironments composed of various cell types such as cancer, immune, stromal and endothelial cells (Hanahan & Weinberg, 2011; Joyce & Fearon, 2015).”
The Principles of Engineering Immune Cells to Treat Cancer (2017, background): “However, in cases where the tumors produce an immunosuppressive environment that directly downregulates T cells (Joyce and Fearon, 2015), it is likely that additional functionality would be required to allow engineered T cells to persist, proliferate, and effectively execute their cytotoxic program.”
Resistance Mechanisms to Immune-Checkpoint Blockade in Cancer: Tumor-Intrinsic and -Extrinsic Factors. (2016, neutral): “…reach malignant cells; and (3) recognize and respond to their target (e.g., lytic granule release by CTLs kills the recognized malignant cell), which requires sufficient tumor cell exposure of peptideMHC complexes and the overcoming of potential immunoregulatory mechanisms (Joyce and Fearon, 2015).”