scholarly journals Correction: Immature dendritic cells navigate microscopic mazes to find tumor cells

Lab on a Chip ◽  
2019 ◽  
Vol 19 (18) ◽  
pp. 3140-3140
Author(s):  
Eujin Um ◽  
Jung Min Oh ◽  
Juhee Park ◽  
Taegeun Song ◽  
Tae-Eon Kim ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tumor Cells ◽  
Immature Dendritic Cells

Correction for ‘Immature dendritic cells navigate microscopic mazes to find tumor cells’ by Eujin Um et al., Lab Chip, 2019, 19, 1665–1675.

scholarly journals Photothermal Ablation of Cancer Cells by Albumin-Modified Gold Nanorods and Activation of Dendritic Cells

Materials ◽  
2018 ◽  
Vol 12 (1) ◽  
pp. 31 ◽  
Author(s):  
Xiuhui Wang ◽  
Jingchao Li ◽  
Naoki Kawazoe ◽  
Guoping Chen
Keyword(s):  
Dendritic Cells ◽  
Tumor Cells ◽  
Gold Nanorods ◽  
Metastatic Cancer ◽  
Cell Interaction ◽  
Soluble Factors ◽  
Photothermal Ablation ◽  
Immature Dendritic Cells ◽  
Direct Cell ◽  
Cell Cell

Nanoparticle-mediated photothermal therapy has been widely studied for cancer treatment. It is important to disclose how photothermally ablated tumor cells trigger immune responses. In this study, bovine serum albumin (BSA)-coated gold nanorods (BSA-coated AuNRs) were prepared and used for photothermal ablation of breast tumor cells. The BSA-coated AuNRs showed high photothermal conversion efficiency and good photothermal ablation effect towards tumor cells. The ablated tumor cells were co-cultured with immature dendritic cells (DCs) through a direct cell contacting model and diffusion model to confirm the stimulatory effects of cell–cell interaction and soluble factors released from ablated tumor cells. The results indicated that photothermally ablated tumor cells induced immune-stimulatory responses of DCs through both cell–cell interaction and soluble factors. The results should be useful for synergistic photothermal-immunotherapy of primary and metastatic cancer.

scholarly journals In Breast Carcinoma Tissue, Immature Dendritic Cells Reside within the Tumor, Whereas Mature Dendritic Cells Are Located in Peritumoral Areas

1999 ◽  
Vol 190 (10) ◽  
pp. 1417-1426 ◽  
Author(s):  
Diana Bell ◽  
Pascale Chomarat ◽  
Denise Broyles ◽  
George Netto ◽  
Ghada Moumneh Harb ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Breast Carcinoma ◽  
Tumor Cells ◽  
Tumor Bed ◽  
Carcinoma Tissue ◽  
Inflammatory Protein ◽  
Immature Dendritic Cells ◽  
Cytokeratin Expression ◽  
Secondary Lymphoid Organs

We have analyzed the presence of immature and mature dendritic cells (DCs) within adenocarcinoma of the breast using immunohistochemistry. Immature DCs were defined by expression of CD1a-, Langerin-, and intracellular major histocompatibility complex class II–rich vesicles. Mature DCs were defined by expression of CD83 and DC-Lamp. Breast carcinoma cells were defined by morphology and/or cytokeratin expression. We demonstrate two levels of heterogeneity of DCs infiltrating breast carcinoma tissue: (a) immature CD1a+ DCs, mostly of the Langerhans cell type (Langerin+), were retained within the tumor bed in 32/32 samples and (b) mature DCs, CD83+DC-Lamp+, present in 20/32 samples, are confined to peritumoral areas. The high numbers of immature DCs found in the tumor may be best explained by high levels of macrophage inflammatory protein 3α expression by virtually all tumor cells. Confirming the immature/mature DC compartmentalization pattern, in vitro–generated immature DCs adhere to the tumor cells, whereas mature DCs adhere selectively to peritumoral areas. In some cases, T cells are clustering around the mature DCs in peritumoral areas, thus resembling the DC–T cell clusters of secondary lymphoid organs, which are characteristic of ongoing immune reactions.

Immature dendritic cells navigate microscopic mazes to find tumor cells

Lab on a Chip ◽  
2019 ◽  
Vol 19 (9) ◽  
pp. 1665-1675
Author(s):  
Eujin Um ◽  
Jung Min Oh ◽  
Juhee Park ◽  
Taegeun Song ◽  
Tae-Eon Kim ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tumor Cells ◽  
Normal Cells ◽  
Immature Dendritic Cells

Imposing physical confinements in the migration tracks of dendritic cells reveals different migratory behaviors towards cancer vs. normal cells.

Stressed apoptotic tumor cells stimulate dendritic cells and induce specific cytotoxic T cells

Blood ◽  
2002 ◽  
Vol 100 (12) ◽  
pp. 4108-4115 ◽  
Author(s):  
Hanping Feng ◽  
Yi Zeng ◽  
Michael W. Graner ◽  
Emmanuel Katsanis
Keyword(s):  
Dendritic Cells ◽  
Tumor Cells ◽  
Cytotoxic T Cells ◽  
Surface Expression ◽  
Interleukin 12 ◽  
Apoptotic Cells ◽  
T Helper 1 ◽  
Immature Dendritic Cells ◽  
Shock Proteins

We have previously reported that stressed apoptotic tumor cells are more immunogenic in vivo than nonstressed ones. Using confocal microscopy we have confirmed our previous observation that heat-stressed apoptotic 12B1-D1 leukemia cells(BCR-ABL+) express HSP60 and HSP72 on their surface. To explore how the immune system distinguishes stressed from nonstressed apoptotic tumor cells, we analyzed the responses of dendritic cells to these 2 types of apoptotic cells. We found that nonstressed and heat-stressed apoptotic 12B1-D1 cells were taken up by dendritic cells in a comparable fashion. However, when stressed apoptotic 12B1-D1 cells were coincubated with immature dendritic cells for 24 hours, this resulted in greater up-regulation of costimulatory molecules (CD40, CD80, and CD86) on the surface of dendritic cells. Moreover, stressed apoptotic 12B1-D1 cells were more effective in stimulating dendritic cells to secrete interleukin-12 (IL-12) and in enhancing their immunostimulatory functions in mixed leukocyte reactions. Furthermore, we demonstrated that immunization of mice with stressed apoptotic 12B1-D1 cells induced the secretion of T helper-1 (TH1) profile of cytokines by spleen cells. Splenocytes from mice immunized with stressed apoptotic cells, but not nonstressed ones, were capable of lysing 12B1-D1 and the parental 12B1 line, but not a B-cell leukemia line, A20. Our data indicate that stressed apoptotic tumor cells are capable of providing the necessary danger signals, likely through increased surface expression of heat shock proteins (HSPs), resulting in activation/maturation of dendritic cells and, ultimately, the generation of potent antitumor T-cell responses.

Dendritic Cells Derived from K562/A02 Cell Line Treated by Recombinant Adenovirus Encoding Human p53

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4928-4928
Author(s):  
Lian-Sheng Zhang ◽  
Lijuan Li
Keyword(s):  
Dendritic Cells ◽  
Multidrug Resistance ◽  
Immune Responses ◽  
Tumor Cells ◽  
P53 Protein ◽  
P53 Gene ◽  
Multidrug Resistant ◽  
Leukemic Cells ◽  
Immature Dendritic Cells

Abstract Purpose Leukemia, a malignant tumor derived from hemotological system, belongs to a malignant clone disease of hemopoietic stem cell. Studies of immunology have indicated a close relationship between occurrence and development of leukemia and immunity of organism. Immunotherapy can completely clear up residual leukemic cells and cure the disease. The occurrence of multidrug resistance ( MDR ) is known for the main barrier of leukemia chemical therapy. And also, dendritic cells ( DCs ) are the most potent antigen-presenting cells for initiating cellular immune responses in vivo. DCs are attractive immunoregulatory cells for cancer immunotherapy, and their efficacy has been investigated in clinical trials. If we can induce multidrug resistant leukemic cell into a DC which is named with multidrug resistant leukemia-derived DC and promote its maturity with effective and harmless drugs, multidrug resistant leukemia-derived DC not only carries the special antigens of leukemia but also can present the special antigens to immune system to kill corresponding leukemic cells. At the same time, it can reverse indirectly leukemic multidrug resistance. Tumor suppressor gene p53 is pivotal in the regulation of apoptosis, and p53-based immunization is an attractive approach to cancer immunotherapy because of the mutant of p53 protein in malignant but not in normal cells. It has been shown that monocyte-derived human dendritic cells transduced with an adenoviral wild-type p53 (wt-p53) construct mediate the antitumor immune responses against p53-overexpressing tumor cells. We examined whether K562/A02 Cells -derived dendritic cells pulsed with the purified full-length wt-p53 protein were also capable of inducing the specific antitumor responses against K562/A02 cells in vitro. Methods P53 gene was transferred to monoclonal K562/A02 cells. P53 gene transcription was detected with RT-PCR. Proliferation test was conducted by using 3H-thymidine (3H-TdR) incorporation. Immature dendritic cells generated in the presence of interleukin-4 and granulocyte/macrophage colony-stimulating factor from K562/A02 cell line were transduced with an wt-p53. Uptake of p53 protein by dendritic cells was assessed by Western blotting. Induction of p53-specific CTL response was also evaluated by the cytotoxic assay against K562/A02 cells. Results Both Western blotting and and immunohistochemical analysis showed the accumulation of p53 protein in immature dendritic cells. T cells obtained from peripheral blood mononuclear cells of healthy volunteers were stimulated with wt-p53 and then applied to the cytotoxicity assay against the target cells-K562/A02. The CTL activity generated by adenoviral wt-p53-transduced dendritic cells was specific for K562/A02 cells. Conclusion Our results indicate that adenoviral wt-p53-transduced dendritic cells could induce the specific antitumor effect against the target tumor cells and that this in vitro model offers a new and more simple approach to the development of p53 and dendritic cellsbased immunogenetherapy. This offers a novel and promising immunogenetherapeutic srtategy to overcome multidrug resistant leukemia in the future.

Release of iC3b from apoptotic tumor cells induces tolerance by binding to immature dendritic cells in vitro and in vivo

2005 ◽  
Vol 55 (1) ◽  
pp. 31-38 ◽  
Author(s):  
Jan Schmidt ◽  
Christoph Klempp ◽  
Markus W. Büchler ◽  
Angela Märten
Keyword(s):  
Dendritic Cells ◽  
Tumor Cells ◽  
Immature Dendritic Cells

Higher CD1a Levels Correlate with PD-L1 Expression and Predict Worse Overall Survival in Triple-Negative Breast Carcinoma

Breast Care ◽  
2021 ◽  
pp. 1-9
Author(s):  
Jian Zheng ◽  
Yuntao Wei ◽  
Xiaoxi Li ◽  
Zhan Shen ◽  
Yong Zhang ◽  
...  
Keyword(s):  
Overall Survival ◽  
Dendritic Cells ◽  
Lymph Node ◽  
Breast Carcinoma ◽  
Triple Negative ◽  
Carcinoma Tissue ◽  
Kaplan Meier ◽  
Immature Dendritic Cells ◽  
Triple Negative Breast Carcinoma ◽  
High Median

Objective: The aim of this study was to measure the expression of PD-L1, CD1a (a marker for immature dendritic cells), and CD83 (a marker for mature dendritic cells) and further examine the associations of PD-L1, CD83, and CD1a with overall survival (OS) in triple-negative breast carcinoma patients. Methods: PD-L1, CD1a, and CD83 expression in breast carcinoma tissues and CD83 expression in lymph node tissues were examined by immunohistochemistry and tissue microarray in 159 patients. Patients were classified into the low, medium, and high PD-L1, CD1a, and CD83 levels. Pearson χ2 test was used to analyze the correlations between PD-L1, CD1a, and CD83. The Kaplan-Meier method was used to calculate the OS. Multivariate analysis was used to identify determinants of 3- and 5-year OS. Results: 25.1, 25.8, and 49.1% of the patients had low, medium, and high PD-L1 levels, respectively. PD-L1 levels significantly correlated with CD1a (r = 0.30409, p < 0.001) and CD83 levels (r = 0.6146, p < 0.001) in breast carcinoma tissue, as well as CD83 levels (r = 0.17508, p = 0.027) in lymph node. The median OS was 83 months (range 12–106), and the 3- and 5-year OS rates were 94.97% (95% CI 91.57–98.37) and 86.79% (95% CI 81.53–92.06), respectively. Moreover, patients with high median CD1a levels had a significantly lower 5-year OS rate (75.6%) than those with low median CD1a levels (93.5%, p = 0.038). Conclusion: PD-L1, CD1a, and CD83 are variably expressed in triple-negative breast carcinoma tissues, and PD-L1 expression correlates with CD1a and CD83. Higher CD1a levels correlate with PD-L1 expression and predict worse OS in triple-negative breast carcinoma.

scholarly journals Cellular cytotoxicity is a form of immunogenic cell death

2020 ◽  
Vol 8 (1) ◽  
pp. e000325 ◽  
Author(s):  
Luna Minute ◽  
Alvaro Teijeira ◽  
Alfonso R Sanchez-Paulete ◽  
Maria C Ochoa ◽  
Maite Alvarez ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Dendritic Cells ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cd8 T Cells ◽  
Immunogenic Cell Death ◽  
Cell Debris ◽  
Tumor Cell Death ◽  
Mhc Multimer

BackgroundThe immune response to cancer is often conceptualized with the cancer immunity cycle. An essential step in this interpretation is that antigens released by dying tumors are presented by dendritic cells to naive or memory T cells in the tumor-draining lymph nodes. Whether tumor cell death resulting from cytotoxicity, as mediated by T cells or natural killer (NK) lymphocytes, is actually immunogenic currently remains unknown.MethodsIn this study, tumor cells were killed by antigen-specific T-cell receptor (TCR) transgenic CD8 T cells or activated NK cells. Immunogenic cell death was studied analyzing the membrane exposure of calreticulin and the release of high mobility group box 1 (HMGB1) by the dying tumor cells. Furthermore, the potential immunogenicity of the tumor cell debris was evaluated in immunocompetent mice challenged with an unrelated tumor sharing only one tumor-associated antigen and by class I major histocompatibility complex (MHC)-multimer stainings. Mice deficient inBatf3,Ifnar1andSting1were used to study mechanistic requirements.ResultsWe observe in cocultures of tumor cells and effector cytotoxic cells, the presence of markers of immunogenic cell death such as calreticulin exposure and soluble HMGB1 protein. Ovalbumin (OVA)-transfected MC38 colon cancer cells, exogenously pulsed to present the gp100 epitope are killed in culture by mouse gp100-specific TCR transgenic CD8 T cells. Immunization of mice with the resulting destroyed cells induces epitope spreading as observed by detection of OVA-specific T cells by MHC multimer staining and rejection of OVA+EG7 lymphoma cells. Similar results were observed in mice immunized with cell debris generated by NK-cell mediated cytotoxicity. Mice deficient inBatf3-dependent dendritic cells (conventional dendritic cells type 1, cDC1) fail to develop an anti-OVA response when immunized with tumor cells killed by cytotoxic lymphocytes. In line with this, cultured cDC1 dendritic cells uptake and can readily cross-present antigen from cytotoxicity-killed tumor cells to cognate CD8+T lymphocytes.ConclusionThese results support that an ongoing cytotoxic antitumor immune response can lead to immunogenic tumor cell death.

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