Abstract
Though present in low numbers, dendritic cells (DCs) are recognized as major players in the control of cancer by adaptive immunity. The roles of cytotoxic CD8+ T-cells and Th1 helper CD4+ T-cells are well-documented in murine models of cancer and associated with a profound prognostic impact when infiltrating human tumors, but less information is known about how these T-cells gain access to the tumor or how they are primed to become tumor-specific. Here, we highlight recent findings that demonstrate a vital role of CD103+ DCs, which have been shown to be experts in cross-priming and the induction of anti-tumor immunity. We also focus on two different mediators that impair the function of tumor-associated DCs: prostaglandin E2 and β-catenin. Both of these mediators seem to be important for the exclusion of T-cells in the tumor microenvironment and may represent key pathways to target in optimized treatment regimens against cancer.
Original language | English |
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Journal | Seminars in Immunopathology |
Volume | 39 |
Issue number | 3 |
Pages (from-to) | 307-316 |
ISSN | 1863-2297 |
DOIs | |
Publication status | Published - 1 Apr 2017 |
Keywords
- Cancer
- CD103
- Dendritic cells
- Immunology
- PGE
- β-catenin