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Review
. 2014;10(11):3224-35.
doi: 10.4161/hv.29857.

Dendritic cell defects in the colorectal cancer

Annalisa Legitimo  1 , Rita Consolini, Alessandra Failli, Giulia Orsini, Roberto Spisni
Affiliations
Review

Dendritic cell defects in the colorectal cancer

"V体育官网" Annalisa Legitimo et al. Hum Vaccin Immunother. 2014.

Abstract

Colorectal cancer (CRC) results from the accumulation of both genetic and epigenetic alterations of the genome. However, also the formation of an inflammatory milieu plays a pivotal role in tumor development and progression. Dendritic cells (DCs) play a relevant role in tumor by exerting differential pro-tumorigenic and anti-tumorigenic functions, depending on the local milieu. Quantitative and functional impairments of DCs have been widely observed in several types of cancer, including CRC, representing a tumor-escape mechanism employed by cancer cells to elude host immunosurveillance. Understanding the interactions between DCs and tumors is important for comprehending the mechanisms of tumor immune surveillance and escape, and provides novel approaches to therapy of cancer. This review summarizes updated information on the role of the DCs in colon cancer development and/or progression. VSports手机版.

Keywords: APC, antigen presenting cells; CRC, Colorectal cancer; CTLA-4, anticytotoxic T-lymphocyte antigen 4; DCregs, regulatory DCs; DCs, dendritic cells; GM-CSF, granulocyte macrophage colony stimulating factor; HMGB, high mobility group box; HNSCC, head and neck squamous cell carcinoma; IFN, interferon; IL, interleukin; MDSCs, myeloid-derived suppressor cells; MHC, major histocompatibility complex; NK,natural killer; PAMP, pathogen-associated molecular pattern; PD-1, programmed death 1; PRRs, pattern recognition receptors; TDLNs, draining lymph nodes; TGF, transforming growth factor; TIDCs, tumor-infiltrating DCs; TLR, toll-like receptor; TNF, tumor necrosis factor; Th, T helper; VEGF, vascular endothelial growth factor; colorectal cancer; dendritic cells; immune response; immunoescape; mDCs, myeloid dendritic cells; pDCs, plasmacytoid dendritic cells; tumor microenvironment V体育安卓版. .

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Figures

Figure 1.
Figure 1.
DC development. This illustration summarizes the current model of the developmental pathways of both myeloid and plasmacytoid DCs. Dashed lines indicate pathways that are likely but not yet definitively shown to operate in DC development. In humans, equivalents of mouse MDP, CDP, and pre-DC have not been found. Cytokines that are important in each transition are indicated. Abbreviations: MPP, multi potential progenitor; CMP, common myeloid progenitor; CLP, common lymphoid progenitor; MDP, macrophage DC progenitor; CDP, common DC progenitor; pre-DC, circulating DC progenitor; pDC, plasmacytoid DC; mDC, myeloid DC; Mo-DC, monocyte-derived DC.
Figure 2.
Figure 2.
Immunophenotypic and functional hallmarks of DC subsets in blood and lymphoid tissue. (A) Both mDC and pDC cells are effective T-cell stimulators and direct the nature of Th responses, although mDC cells primarily induce Th1 differentiation, whereas pDC cells mainly promote a Th2 response. The archetypical antigen/cytokine of each subset is marked in bold. (B) Key cytokines involved in the DC-mediated polarization of naïve T cells into different T-cell subsets. Mature dendritic cells polarize naive Th0 cells into different Th effector cells through several signals: antigen presentation to the T-cell receptor, co-stimulatory signal and secretion of cytokines. Immature dendritic cells prime Th0 cells to make Treg cells. Abbreviations: pDC, plasmacytoid DC; mDC, myeloid DC; Lin, lineage markers; PRRs, pattern-recognition receptors; TLR, Toll like receptors Th, T helper cell; Treg, regulatory T cell; Ag, antigen, TCR, T-cell receptor; CTLA-4, cytotoxic T-lymphocyte antigen 4.
Figure 3.
Figure 3.
Tumor-altered DC function. Tumor-secreted factors can inhibit DC maturation. Immature DCs, displaying low NF-kB activation, low MHC class II and co-stimulatory molecule expression, are defective antigen presenting cells and induce T cell anergy and exhaustion. Tumor-derived factors can also induce the development of immunosuppressive regulatory DCs, which suppress T cell function through multiple mechanisms. More informations regarding the mechanisms by which tumors alter DC function and suppress host anti-tumor immunity are illustrated in the review of Hargadon. Abbreviations: iDC, immature DC; MDC, mature DC; Reg DC, regulatory DC; Treg, regulatory T cell; PD-1L, programmed death 1 ligand.
Figure 4.
Figure 4.
The immune checkpoints CTLA-4 and PD-1/PD-L1. Inhibitory receptors such as anti-cytotoxic T-lymphocyte antigen 4 and programmed death 1 expressed on tumor-specific T cells lead to compromised activation and suppressed effector functions such as proliferation, cytokine secretion, and tumor cell lysis. Modulating these receptors using monoclonal antibodies, an approach termed “immune checkpoint blockade,” has gained momentum as a new approach in cancer immunotherapy. Abbreviations: CTLA-4, cytotoxic T-lymphocyte antigen 4; PD-1, programmed death 1.
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