Several lines of evidence

suggest that DCs loaded with various tumor antigens, such as tumor fragments or antigen peptides, or with antigen genes by way of retrovirus or adenovirus vectors, are capable of activation and expansion of tumor-specific T cells in vitro [5, 13–15]. To date, only a few clinical trials of DC vaccination have been reported in cancer patients, with disappointing results. In addition to the immunodeficiency find more of the patients, several other limitations are currently hindering the potential of this technique, including attaining pure DCs, loading the DCs with tumor antigen, and transducing the DCs with tumor genes [5, 14, 16–18]. DCs, as the most potent antigen presenting cells, play a central role in the initiation and regulation of immune responses, Which are detected using multicolor flow cytometry, electron microscope or immunocytochemistryImmunocytochemistry Immunocytochemistry Immunocytochemistry and so on. However, human DCs are not a homogenous population. Besides inducing anti-tumor immunity, DCs can induce tumor-special anergy or tolerance [18–21]. DCs originate from CD34+ hematopoietic stem cells (HSC). Myeloid dendritic cells (DC1) and plasmacytoid DCs (DC2) are the two principal subpopulations of human DCs, and their characteristics vary greatly in phenotype, migration, and function. DC1 cells are effective T cell stimulators, inducing

CAL-101 ic50 a tumor specific immune response; however, the function of DC2 cells is uncertain. They not only stimulate tumor specific immune responses, they also contribute to tumor immune tolerance. It has been suggested that CD11c+DC1 cells primarily induce Th1 differentiation, Cediranib (AZD2171) whereas DC2 cells, which express the receptor for IL-3 (CD123), mainly promote a Th2 response. Many studies indicate that in a tumor microenvironment, DCs both decrease in quantity and are impaired in function. Both DC populations were significantly lower in patients with cancer than in healthy

donors [22–25]. DC subsets may be used differentially in immune responses to various antigens, including tumor-associated antigens. However, little is known about the frequency or function of these two subsets of DCs in cervical carcinoma patients. Tumors lack specific antigens and can hide or change their antigens to escape immune surveillance. They can also manipulate dendritic cell subset distributions and subvert tumor immunity by secreting Ralimetinib inhibitory cytokines such as IL-2, IL-4, IL-10, IL-6, TFG-β, VEGF, and IFN-γ. Some of these are produced by human tumor cells themselves, whereas others are not only produced by tumor cells but also induced systemically by tumor cell-derived products. TGFβ acts as a stimulator of tumor invasion by promoting extracellular matrix production and angiogenesis, stimulating tumor proliferation, and inhibiting host immune functions [26]. IL-6 has an immunosuppressive role in cancer patients by inhibiting the development of DCs [27].