| Background Ovarian carcinoma is one of the commonest cancers amonggynecological malignancies. Two thirds of patients with ovarian carcinoma present advanced-stage disease at the first diagnosis and have poor prognosis because of extensive metastasis of cancer cells and rapidly accumulating ascetic fluid. Ovarian carcinoma remains confined to the abdominopelvic region even in advanced stages of the disease, which suggests that the growth of this malignancy may be related to local immunosuppression. It's certain that there are local immunodeficiency by analysis of concentration of cytokine and phenotype of lymphocytes from ascetic fluid and tumor tissues of patients with ovarian carcinoma. Several mechanisms responsible for immune deficiency have been suggested, including lack or modulation of tumor antigen; secretion of tumor-derived inhibitory factor and activation of inhibitory regulatory elements of the immune system; or tolerance and deleting of antigen presentation of ovarian tumor cells. Increasing evidences support the notion that both immune activation and immune suppression depend on antigen presentation by antigen presenting cells (APC), APC play an important role in initiating the antitumor immune response. Dendritic cell (DC) is the most potent professional APC. DC captures andprocesses the antigen into small pieces of peptides, then presents the peptides to T cells with the help of co-stimulatory molecules and adhesion molecules via the MHC pathway, which ultimately activates T cells to mediate immune responses against tumor. DC can infiltrate into the tumor tissue under stimulation of various signals within the tumor microenvironment, which is named as tumor infiltrating dendritic cell (TIDC). Tumor infiltrated by DC reflects the interaction between a developing tumor and the host immune system. Several studies have indicated that a correlation between DC infiltration and the prognosis of patients with malignant neoplasms, including colorectal cancer, thyroid carcinoma, lung cancer ,oral carcinoma etc. It indirectly reflects that there is a close relationship between TIDC and the host immune system. But earlier studies reported that some of TIDC are immature DC, which express reduced co-stimulatory molecule CD80,CD86, adhesion molecule CD40, CD54 and antigen presenting complexes MHC . These immature DCs fail to provide two recognition signals that is necessary to stimulate T lymphocytes effectively and induce a state of T lymphocytes anergy. It has been reported that some soluble cytokine such as VEGF, IL-10,TGF-b can inhibit DC maturation and block DC development in vitro. VEGF binds to two primary receptors Flt-1 and KDR, which are expressed by CD34+ hematopoetic progenitor cells. VEGF causes a defect in the functional maturation of DC from progenitors and induces DC apoptosis in vitro. This developmental defect is associated with activation of transcription factor NF-kappaB, which is transduced via a nontyrosine kinase-dependent pathway. VEGF levels in the tumor tissue, ascites and sera of ovarian carcinoma are higher and popularly considered to be involved in an enhancement of angiogenesis and microvascular permeability. But it's still unclear whether VEGF is an immune inhibitor that suppresses both the development and maturation of DC in ovarian carcinoma, causes a defective local antitumor immune response, and allows tumor cells to escape immune system and metastasize extensively in the abdominal cavity. DCs express three markers, S-100, CDla and CD83. S-100 is aDC identification marker in clinical tissue samples; CDla is a particular marker of human DC, which only processes and presents nonpeptide foreign lipid and glycolipid antigens to T cells; CD83 is a marker of mature DC. In this study, we detected TIDC density and phenotype, the expression levels of VEGF in ovarian carcinoma .Our objective is to investigate the role of TIDC in local immunity of ovarian carcinoma and the role of VEGF inhibiting in the function of TIDC. This study probably provide an exper...
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