الفهرس 
Epidemiology
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Abstract
Dendritic cells (DCs) are the most effective professional antigen presenting cells (APCs) of the immune system. These cells are in charge of bridging the gap between innate and adaptive immunity, including the activation of anti-tumor T cells. (Gardner et al., 2020).
They recognise , process and present tumor associated antigens by major histocompatibility complexes (MHCs), and subsequently trigger a CD4+ and CD8+ T cell response (Szpor et al., 2021). They can also present lipid antigens by non-classical CD1 molecules that activate natural killer T (NKT) cells (Martinek et al., 2019). They are developed from their precursors in bone marrow (BM) via a series of steps involving common myeloid progenitors (CMP). CMPs differentiate into a common dendritic cell progenitor (CDP), which gives rise to plasmacytoid and conventional dendritic cells (cDCs) (Gardner et al., 2020).
Immature DCs have high endocytic activity and a low level of T lymphocytes activation, so they probably encourage antigen-specific tolerance rather than immunity (Szpor et al., 2021). Upon contact with the antigen, these immature DCs are activated into mature DCs and migrate to the lymphoid tissues where they activate T lymphocytes, thus generating an antigen-specific immune response.
Depending on their type, the level of maturation as well as the functional state of DCs can increase effector T cell responses (good prognosis) or mediate T cell tolerance (increase tumour progression).
DC maturation is associated with:
(1) A reduction in antigen-capture activity.
Chapter I
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Introduction
(2) The chemokine receptor -7 (CCR7) is expressed on the surface of DCs, allowing them to migrate into draining lymph nodes.
(3) Co-stimulatory molecules are transported to the cell surface using peptide-MHC (pMHC) complexes.
(4) The capacity to produce cytokines that aid T cell development, such as IL-12 and IL-15.
Tumors and their microenvironment (TME) influence the immune system to prolong their survival and development. DC functions have been discovered to be disrupted in a number of ways. For example, tumor-infiltrating DCs that highly express programmed death-ligand1 (PD-L1), inhibit T-cell activation and cytokine production, leading in TME immunosuppression. PD-1/PD-L1 blockage restores DC activity (Salmon et al., 2016).
In advanced inoperable cancers, PD-1 receptor or PD-L1 ligand blockade on immune cells or tumour cells can mediate cancer resistance to conventional treatment approaches (Yarchoan, Hopkins et al. 2017). According to recent retrospective research, advanced melanoma, renal cell carcinoma or non-small cell lung carcinoma patients with low tumor burden were more likely to have long-term survival after anti–PD-1 therapy (Topalian et al., 2019). The overexpression of the TIM-3 (T-cell immunoglobulin and mucin domain-containing-3) protein on DCs is another mechanism by which DCs function is disrupted (de Mingo Pulido et al., 2018).
Epigenetic dysregulation also provides several mechanisms for cancer development and progression due to its effects on the aberrant activation of oncogenes and repression of tumor suppressor genes.