Academic literature on the topic 'Cell Immunotherapy'

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Journal articles on the topic "Cell Immunotherapy"

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McKee, Mark, D. "T cell immunotherapy." Frontiers in Bioscience 12, no. 1 (2007): 919. http://dx.doi.org/10.2741/2114.

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Sabado, Rachel Lubong, and Nina Bhardwaj. "Dendritic cell immunotherapy." Annals of the New York Academy of Sciences 1284, no. 1 (May 2013): 31–45. http://dx.doi.org/10.1111/nyas.12125.

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Osada, Takuya, Timothy M. Clay, Christopher Y. Woo, Michael A. Morse, and H. Kim Lyerly. "Dendritic Cell-Based Immunotherapy." International Reviews of Immunology 25, no. 5-6 (January 2006): 377–413. http://dx.doi.org/10.1080/08830180600992456.

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Velardi, Andrea. "NK cell adoptive immunotherapy." Blood 105, no. 8 (April 15, 2005): 3006. http://dx.doi.org/10.1182/blood-2005-01-0322.

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Sabado, Rachel L., Sreekumar Balan, and Nina Bhardwaj. "Dendritic cell-based immunotherapy." Cell Research 27, no. 1 (December 27, 2016): 74–95. http://dx.doi.org/10.1038/cr.2016.157.

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Lee, Jong-Hoon, and Harvey G. Klein. "Mononuclear Cell Adoptive Immunotherapy." Hematology/Oncology Clinics of North America 8, no. 6 (December 1994): 1203–22. http://dx.doi.org/10.1016/s0889-8588(18)30130-8.

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Feldmann, Marc, Carl H. June, Andrew McMichael, Ravinder Maini, Elizabeth Simpson, and James N. Woody. "T-cell-targeted immunotherapy." Immunology Today 13, no. 3 (January 1992): 84–85. http://dx.doi.org/10.1016/0167-5699(92)90146-x.

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Razzak, Mina. "New cell-based immunotherapy?" Nature Reviews Urology 9, no. 3 (February 21, 2012): 122. http://dx.doi.org/10.1038/nrurol.2012.18.

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Bakulesh, Khamar. "Immunotherapy of Bladder Cancer." Cancer Medicine Journal 3, no. 2 (December 31, 2020): 49–62. http://dx.doi.org/10.46619/cmj.2020.3-1020.

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Bladder cancer used to be the only cancer treated by immunotherapy in form of intravesical BCG. Since approval of BCG for Non muscle invasive bladder cancer (NMIBC), there has been significant advancement in our knowledge about immune alteration in cancer and availability of immunotherapeutic agents. Tumor induced cell mediated immunosuppression is identified as a key factor for development and progression of cancer. Immune suppression in bladder cancer is predominantly through Macrophages. Myeloid derived suppressor cell, NK cells, Treg and expression of immune checkpoint receptor inhibitors also contribute to immune suppression. BCG induces innate immune response and its efficacy is limited to NMIBC. Novel immunotherapeutic agents evaluated in bladder cancer are administered locally or systemically to induce innate or adaptive immune response. Systemic administration of antibodies against PD-1/PD-L1 axis are now approved for treatment of locally advanced/metastatic bladder cancer as a first line as well as second line therapy. Pembrolizumab is also approved for BCG unresponsive NMIBC. Since response to immunotherapy are neither uniform nor universal, attempts are made to identify prognostic and predictive biomarkers. Identified biomarkers lack desired specificity and sensitivity. Several immune approaches using innate as well as adaptive mechanism are under evaluation to improve outcome of intravesical BCG or immune check point receptor inhibitors.
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Y, Elshimali. "Chimeric Antigen Receptor T-Cell Therapy (Car T-Cells) in Solid Tumors, Resistance and Success." Bioequivalence & Bioavailability International Journal 6, no. 1 (2022): 1–6. http://dx.doi.org/10.23880/beba-16000163.

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CARs are chimeric synthetic antigen receptors that can be introduced into an immune cell to retarget its cytotoxicity toward a specific tumor antigen. CAR T-cells immunotherapy demonstrated significant success in the management of hematologic malignancies. Nevertheless, limited studies are present regarding its efficacy in solid and refractory tumors. It is well known that the major concerns regarding this technique include the risk of relapse and the resistance of tumor cells, in addition to high expenses and limited affordability. Several factors play a crucial role in improving the efficacy of immunotherapy, including tumor mutation burden (TMB), microsatellite instability (MSI), loss of heterozygosity (LOH), the APOBEC Protein Family, tumor microenvironment (TMI), and epigenetics. In this minireview, we address the current and future applications of CAR T-Cells against solid tumors and their measure for factors of resistance and success.
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Dissertations / Theses on the topic "Cell Immunotherapy"

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Opel, Cary F. (Cary Francis). "T cell mediated combination immunotherapy." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/107075.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Chemical Engineering, February 2016.
Cataloged from PDF version of thesis. "September 2015."
Includes bibliographical references (pages 128-131).
Immunotherapy is a broad treatment strategy that harnesses the immune system to fight off a particular condition or disease. Cancer immunotherapy is the specific application of agents designed to interact or stimulate the immune system to fight off tumors. Treatments as diverse as passive antibody therapy, cytokine support, and comprehensive adoptive T cell transfer make up the broad field of immunotherapeutics. Due to the naturally complex interactions inherent in the immune system, there are many options for therapeutic intervention, however, this same complexity makes it extremely difficult to optimize treatment strategies. Because of this, research into developing new immunotherapies, optimizing existing immunotherapies, and designing new combinations of immunotherapies is still critical in the fight against cancer. Although there have been ongoing successes of individual immunotherapies in the clinic, the complexity and interdependence of the immune system suggests that any single therapeutic intervention will be insufficient to reject established malignancies. Increased interest in applying combinations of immunotherapies in the clinic requires more thorough preclinical work to guide the designs of these studies. The work presented in this thesis focuses on developing combinations of immunotherapies to treat preclinical models of cancer, as well as studying the underlying mechanism of tumor control. T cells are potent mediators of cytotoxicity and when properly used in adoptive cell transfer (ACT) protocols, can be highly effective in the treatment of cancer. ACT consists of three steps: 1) harvesting and purifying T cells from the patient, 2) enriching or modifying the T cells to become tumor specific, and 3) reinfusing the T cells along with supporting therapies. Therapies given alongside ACT are often adjuvants designed to enhance T cell response. However, focusing therapies only on enhancing the activity of the transferred T cells may miss out on synergistic effects when other parts of the immune system are simultaneously engaged. To study the effect of adjuvant therapy on ACT, a preclinical murine model was analyzed. Large, established B16F10 tumors were controlled when pmel-1 T cells were given with a course of supportive MSA-IL2 cytokine therapy, however, no cures were observed. When a course of TA99 antibody therapy was added alongside ACT, a high rate of cures was observed. Flow cytometry of both circulating and tumor infiltrating pmel-1 cells showed massive expansion and activation. Additionally, tumor infiltration of neutrophils, NK cells, and DCs were greatly enhanced by adjuvant therapy. DCs in the tumor draining lymph nodes were largely unchanged by the therapies. Engagement of the humoral immune response was also observed in both treatment cases. Surprisingly, antibody therapy did not substantially alter any of the mechanistic observations made in this study, despite its critical role in achieving cures of tumors. While ACT is a highly effective therapy, its clinical applicability is hindered by the complexity of performing T cell transplants and manipulations. A more optimal solution would involve purely injectable treatments that could elicit the same level of tumor specific T cell response in conjunction with potent recruitment of the adaptive immune system against tumors. To achieve this, working in collaboration with the Irvine Lab, combinations of immunotherapy using up to four different components were tested to identify critical factors in the successful rejection of established tumors in preclinical models. The four components of tumor targeting antibody, cytokine support, checkpoint blockade, and cancer vaccine acted synergistically to reject tumors from B16F10, TC-1, and DD-Her2/neu cell lines. The cancer vaccine elicited large numbers of tumor-specific T cells, and acted as a replacement for ACT. By analyzing subset combinations of this full treatment, the roles of each therapeutic component were identified. CD8 T cells and cross-presenting DCs were critical to curing subcutaneous tumors. Cytokine therapy was indispensable for effective tumor control, promoted immune cell infiltration into the tumor, and led to an increase in DCs. In combination with the other therapies, vaccination against a tumor antigen elicited a strong immunological memory response that was able to reject subsequent tumor rechallenge, as well as promote antigen spreading to new epitopes. Successful combinations were demonstrated to be dependent on the recruitment of both the adaptive and innate branches of the immune system. Finally, the efficacy of this combination of treatments was demonstrated by controlling the growth of induced tumors in a BRaf/Pten model. Combination immunotherapy promises a future where synergistic treatments are specifically tailored to individual cancers leading to highly effective responses. However, determining the optimal combination of therapies, the complexity of dosing strategies, and the availability of targeted treatments are all barriers that must be overcome. The analysis presented here will make a significant contribution to the body of knowledge on immunotherapy as it has shown the importance of combining orthogonal immunotherapies in order to get durable cures to established tumors. These results will hopefully encourage combinations of orthogonally acting therapies based on T cells to achieve stronger clinical responses. By determining the necessary requirements for a strong, synergistic response to tumorous growths, more effective combination immunotherapy protocols may be designed in the future.
by Cary F. Opel.
Ph. D.
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Goddard, Ruth Victoria. "Generation of in vitro B-cell chronic lymphocytic leukaemia-specific T cell responses using dendritic cells." Thesis, University of Plymouth, 2002. http://hdl.handle.net/10026.1/2695.

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Immunotherapy using dendritic cells has shown encouraging results in both haematological and non-haematological malignancies. In this study, monocyte-derived dendritic cells from patients with B-cell Chronic Lymphocytic Leukaemia were generated by culture in Interleukin-4 and Granulocyte Macrophage-Colony Stimulating Factor. Lysate-pulsed autologous dendritic cells were used as antigen presenting cells in co-culture with autologous B-cell Chronic Lymphocytic Leukaemia T-cells. B-cell Chronic Lymphocytic Leukaemia T-cells stimulated with B-cell Chronic Lymphocytic Leukaemia lysate-pulsed autologous dendritic cells showed a significant increase in cell surface expression of Interleukin-2 Receptor (CD25), Interferongamma secretion and cytotoxicity against autologous B-cell Chronic Lymphocytic Leukaemia B-cell targets hut not against targets from healthy volunteers. Responses were only stimulated by the B-cell Chronic Lymphocytic Leukaemia B cell lysate. Cytotoxicity was Major Histocompatibility Complex Class II restricted. The addition of maturation agents such as Lipopolysaccharide, Tumour Necrosis Factor-alpha and Polyriboinosinic Polyribocytidylic Acid to monocyte derived dendritic cells was unsuccessful at increasing anti-tumour responses. Pre-treatment of T cells with Interleukin-15 before stimulation by lysate pulsed autologous dendritic cells increased numbers of activated cells, cytokine secretion and specific cytotoxicity to B-cell Chronic Lymphocytic Leukaemia 8-cells. Fusion of monocyte derived dendritic cells and B-cell Chronic Lymphocytic Leukaemia B-cells generated both Major Histocompatibility Complex Class I and Class II restricted cytotoxicity to B-cell Chronic Lymphocytic Leukaemia B-cell targets. When B-cell lysates were analysed using reducing sodium dodecyl sulphate-polyacrylamide gel electrophoresis, a B-cell Chronic Lymphocytic Leukaemia specific hand at 42,000 Dalton and other patient specific bands were observed. Only the 65,000 Dalton and 42,000 Dalton hands were capable of stimulating comparable T cell responses as the whole lysate. The 65,000 Dalton band from normal healthy volunteers showed a dominant peptide that closely matched Human Serum Albumin. The 42,000 Dalton band from B-cell Chronic Lymphocytic Leukaemia patients showed a possible match with Human Actin.
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Wurzenberger, Cornelia. "Dendritic cell vaccines in tumor immunotherapy." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-95530.

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Harley, Eric. "Modeling Cancer Cell Response to Immunotherapy." Scholarship @ Claremont, 2004. https://scholarship.claremont.edu/hmc_theses/164.

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Significant work has been done modeling cancerous tumor growth and response to therapy under certain simplifying assumptions, specifically, the assumption of spatial homogeneity. We have chosen a spatially heterogenous model for cancer cell growth using a hybrid Lattice-Gas Cellular Automata method. Cell mitosis, apoptosis, and necrosis are explicitly modeled along with the diffusion of nutrients and a necrotic signal. The model implementation is verified qualitatively and is modified to execute on a parallel computer.
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Lute, Kenneth D. "Costimulation and tolerance in T cell immunotherapy." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141850521.

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White, Matthew. "T-cell cancer immunotherapy : characterisation and manipulation of tumour antigen-specific T cell subsets for adoptive immunotherapy in mouse models." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9148.

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Understanding the behaviour of T cells in context of tumour responses is crucial for designing adoptive immunotherapy strategies. The aim of the study is to characterise tumour-specific T cells, including conventional and regulatory T cells (Tregs), in tumour-bearing mice after adoptive transfer. Male-specific minor histocompatibility antigen HY was used as the tumour-associated antigen, expressed by MB49 murine bladder carcinoma and recognised by TCR transgenic CD4 (Marilyn) and CD8 (Matahari) T cells. Unlike male skin grafts, MB49 tumours express a panel of immune-suppressive molecules including PD-L1, FAS-L, TGF-β, IL-10 and IDO which contribute to the formation of a tolerogenic microenvironment. As a result, HY-specific CD8 T cells reject syngeneic male skin grafts but not MB49 tumours. In response to MB49 tumours, HY-specific Tregs underwent expansion. A fraction of proliferating Tregs also lost FoxP3 and became ex-Tregs, which upregulated IFNγ, and downregulated a panel of Treg-specific genes. In addition, it was observed that preferential ex-Treg differentiation took place in an IL-6-enriched microenvironment, such as in the mesenteric lymph nodes. The antigen-specific CD8 response to MB49 is insufficient for rejection. Retroviral modification of MB49 to express hIL-2 allows for induction of effective antigen-specific CD8 responses, providing a potent whole cell in vivo vaccine strategy for exploring factors mediating immune evasion. Finally, the role of anti-HY TCR transgenic T cells in GvHD is assessed. Lymphopenic male recipients lose weight after adoptive transfer of CD4 but not CD8 T cells. With radiation preconditioning, full-blown GvHD ensues, raising questions about this combination for clinical therapy. This study advances knowledge of antigen-specific T effector and Treg responses to HY in a range of environments, including MB49 tumours, male skin grafts and GvHD. It highlights the importance of understanding not only induction of effector responses, but potentially harmful side-effects of adoptive cell transfer.
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Cabezón, Cabello Raquel. "Tolerogenic dendritic cell-based immunotherapy in Crohn’s disease." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/310604.

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The quality of life of a significant proportion of IBD patients is poor as a result of persistent disease activity and repeated surgery, among others. Current treatments for Crohn’s disease are not able to neither prevent this serious impact nor improve the long term prognosis of a significant proportion of patients. Therefore, new therapeutic approaches are needed in order to modify the immune response of these patients. We hypothesize that administration of ex-vivo generated autologous tol-DCs to Crohn’s disease patients may arrest Th1 lymphocyte proliferation and therefore may restore specific tolerance against non-pathogenic antigens in the gut. The overall objective of this thesis was to generate and characterize tol-DCs for the purpose of implementing an autologous immunotherapy treatment for Crohn’s disease patients. In the first study, we described the generation of tol-DCs from healthy donors and Crohn’s disease patients by use of clinical-grade reagents in combination with dexamethasone as immunosuppressive agent and characterized their functional properties. Our main findings demonstrated that the combination of dexamethasone with a specific cytokine cocktail yields clinical-grade DCs with the following characteristics: a semi-mature phenotype, a pronounced shift towards anti-inflammatory versus inflammatory cytokine production and low T-cell stimulatory properties. This characteristic tolerogenic profile is maintained when tol-DCs are activated using heat-inactivated Gram-negative bacteria as maturative stimulus. Whole microorganisms contain multiple PAMPs capable of stimulating DCs by different pathways. Our results clearly showed a strong inhibitory effect on DC phenotype, a robust inhibition of pro-inflammatory cytokines, increased IL-10 secretion, and inhibition of T-cell proliferation and Th1 induction. Interestingly, we showed that tol-DCs have reduced immunogenic capacity in autologous, allogeneic and antigen-specific T-cell responses. We further evaluated the ability of tol-DCs to induce CD4+ T-cell hypo-responsiveness. Our results demonstrated that T-cells or antigen-specific T-cells previously cultured with tol-DCs are anergic exhibiting a reduced capacity to proliferate as well as reduced IFN-gamma secretion when rechallenged with fully competent mDCs. With regard to tol-DCs clinical application, we importantly found that their tolerogenic properties remain stable after washing out dexamethasone and subsequent restimulation with LPS, CD40L or different Gram-negative enterobacteria strains. All these properties led us to conclude that this cell product is suitable to be tested in clinical trials of immune-based diseases such as Crohn’s disease. We further identified a positive biomarker for tol-DCs, MERTK receptor is highly expressed on clinical grade dexamethasone-induced human tol-DCs and contributes in their tolerogenic properties. Our results demonstrated that MERTK expression in human DCs is regulated by glucocorticoids and described a new function of this receptor in directly regulating T-cell response. Interestingly, our findings showed that neutralization of MERTK with monoclonal antibodies in allogeneic MLR cultures leads to increased T-cell proliferation and IFN-gamma production. The direct regulation of T-cell response was confirmed by the use of recombinant MERTK-Fc protein, used to mimic MERTK on DCs. Our results remarkably showed that MERTK-Fc suppresses naïve and antigen-specific memory Tcell proliferation and activation. These findings identified a new non-cell autonomous regulatory function of MERTK expressed on DCs. Additionally, we described that this regulation is mediated by the neutralization of MERTK soluble ligand PROS1. We also found that MERTK is expressed on T-cell surface and that PROS1 drives an autocrine pro-proliferative effect on these cells. In summary, the results of this work demonstrated that MERTK on DCs regulates T-cell activation and expansion through the competition for PROS1 interaction with MERTK in the T-cells. We showed that MERTK expression in human DCs has a key role in instructing adaptive immunity and identified MERTK as a potent suppressor of T-cell response. Therefore targeting MERTK may provide an interesting approach to effectively increase or suppress tolerance for the purpose of immunotherapy.
Esta tesis doctoral estudia el proceso de generación de células dendríticas tolerogénicas en grado clínico, con el objetivo de establecer un protocolo destinado al tratamiento de la enfermedad de Crohn. El estudio realizado ha permitido la caracterización de dichas células y sus propiedades tolerogénicas, incluyendo la descripción novedosa de un marcador de células tolerogénicas y el estudio de sus propiedades funcionales relacionadas con la inducción de tolerancia.
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Vertuani, Simona. "Strategies to optimize T cell-based cancer immunotherapy /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-891-6/.

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Adikari, Sanjaya Bandara. "Cytokine-modulated dendritic cell immunotherapy in autoimmune diseases /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-149-0/.

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Jackson, Andrew Mark. "Cytokines, cell adhesion molecules and bladder cancer immunotherapy." Thesis, University of Edinburgh, 1993. http://hdl.handle.net/1842/19867.

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The intravesical administration of Bacillus Calmette Guerin for the treatment of transitional cell carcinoma of the bladder is the most effective immunotherapy for any solid human malignancy. Despite this awesome accolade relatively little is understood of its mechanism of action. This study details the in vitro interaction between IL-2 activated lymphocytes and tumour cells, the effect of cytokines produced as a result of immunotherapy on tumour cells and the relationship of these findings to the situation in vivo. Bladder cancer cells were not found to be susceptible to NK cell activity but were found to be differentially susceptible to IL-2 activated lymphocytes. No correlation was evident between the histopathological grade of the tumour. The interaction between these cells was observed to involve intimate contact and the tumour cells were found to constitutively express either ICAM-1 or ICAM-2. The expression of these cell adhesion molecules correlated significantly with the sensitivity of the tumour cells to LAK mediated cytolysis. Following BCG therapy a variety of cytokines including IFNγ and TNFα are detected in the urine. When bladder cancer cells were cultured in the presence of recombinant IFNγ and TNFα an increase in the levels of ICAM-1 expression was observed. The optimal stimulation was found after 24 hours culture with 100Uml-1 IFNγ, whilst TNFα stimulated to a lesser extent. Culture in the presence of both cytokines was observed to synergistically induce or augment ICAM-1 expression. Following culture with IFNγ, the tumour cells displayed increased susceptibility to LAK activity, this was significantly correlated with increased ICAM-1 expression. The levels of tumour cell response to IFNγ could not be correlated with either the abundance or affinity of specific receptors as determined by Scatchard analysis. Thus investigations were initiated into the events down-stream of the ligand-receptor interaction. Monoclonal antibodies to ICAM-1, decreased the sensitivity of tumour cells to LAK activity. However, monoclonal antibodies to LFA-1 (the ligand for ICAM-1) further blocked the action of LAK cells.
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Books on the topic "Cell Immunotherapy"

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Katz, Samuel G., and Peter M. Rabinovich, eds. Cell Reprogramming for Immunotherapy. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0203-4.

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Debruyne, Frans M. J., Ronald M. Bukowski, J. Edson Pontes, and Pieter H. M. de Mulder, eds. Immunotherapy of Renal Cell Carcinoma. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75853-9.

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1955-, Klein Eric A., Bukowski Ronald M, and Finke James H. 1944-, eds. Renal cell carcinoma: Immunotherapy and cellular biology. New York: Marcel Dekker, Inc., 1993.

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1950-, Morstyn George, and Sheridan William 1954-, eds. Cell therapy: Stem cell transplantation, gene therapy, and cellular immunotherapy. Cambridge: Cambridge University Press, 1996.

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Debruyne, F. M. J., 1941- and Ackermann R. 1941-, eds. Immunotherapy of renal cell carcinoma: Clinical and experimental developments. Berlin: Springer-Verlag, 1991.

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Burkhard, Ludewig, and Hoffmann Matthias W, eds. Adoptive immunotherapy: Methods and protocols. Totowa, N.J: Humana Press, 2005.

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N, Winter Jane, ed. Blood stem cell transplantation. Boston: Kluwer Academic Publishers, 1997.

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M, Bukowski Ronald, Finke James H. 1944-, and Klein Eric A. 1955-, eds. Biology of renal cell carcinoma. New York: Springer-Verlag, 1995.

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Donnadieu, Emmanuel, ed. Defects in T Cell Trafficking and Resistance to Cancer Immunotherapy. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42223-7.

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1956-, Zhang Jingwu, and Cohen Irun R, eds. T-cell vaccination. New York: Nova Biomedical Books, 2008.

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Book chapters on the topic "Cell Immunotherapy"

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Shaffer, Donald R., Conrad Russell Y. Cruz, and Cliona M. Rooney. "Adoptive T Cell Transfer." In Cancer Immunotherapy, 47–70. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4732-0_3.

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Wilke, Cailin Moira, Shuang Wei, Lin Wang, Ilona Kryczek, Jingyuan Fang, Guobin Wang, and Weiping Zou. "T Cell and Antigen-Presenting Cell Subsets in the Tumor Microenvironment." In Cancer Immunotherapy, 17–44. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4732-0_2.

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Gottschalk, S., C. M. Bollard, K. C. Straathof, C. U. Louis, B. Savoldo, G. Dotti, M. K. Brenner, H. E. Heslop, and C. M. Rooney. "T Cell Therapies." In Immunotherapy in 2020, 69–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/2789_2007_039.

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Deschoolmeester, Vanessa, David Kerr, Patrick Pauwels, and Jan B. Vermorken. "Cell Based Therapy: Modified Cancer Cells." In Immunotherapy for Gastrointestinal Cancer, 23–46. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43063-8_2.

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DeSantes, Kenneth, and Kimberly McDowell. "NK Cell and NKT Cell Immunotherapy." In Immunotherapy for Pediatric Malignancies, 175–215. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43486-5_9.

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Motohashi, Shinichiro. "NKT Cell-Based Immunotherapy." In Immunotherapy of Cancer, 75–86. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55031-0_6.

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Plautz, Gregory E., Peter A. Cohen, David E. Weng, and Suyu Shu. "T-Cell Adoptive Immunotherapy." In Handbook of Cancer Vaccines, 359–76. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-680-5_24.

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Gottschalk, Stephen, and Cliona M. Rooney. "Adoptive T-Cell Immunotherapy." In Epstein Barr Virus Volume 2, 427–54. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22834-1_15.

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Berger, T. G., and E. S. Schultz. "Dendritic Cell-Based Immunotherapy." In Current Topics in Microbiology and Immunology, 163–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-06508-2_8.

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François, Moïra, and Jacques Galipeau. "Mesenchymal Stromal Cells: An Emerging Cell-Based Pharmaceutical." In Experimental and Applied Immunotherapy, 127–48. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-980-2_6.

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Conference papers on the topic "Cell Immunotherapy"

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Dimitriu, Gabriel, Vasile lucian Boiculese, Mihaela Moscalu, and Cristina gena Dascalu. "GLOBAL SENSITIVITY ANALYSIS APPLIED TO A CANCER IMMUNOTHERAPY MODEL." In eLSE 2019. Carol I National Defence University Publishing House, 2019. http://dx.doi.org/10.12753/2066-026x-19-177.

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Sensitivity analysis methods have a long history and have been widely applied in different fields, such as environmental modeling, economical modeling for decision making, parameter estimation and control, chemical kinetics, and biological modeling analysis, with metabolic networks, signaling pathways and genetic circuits. Cancer immunotherapy is based on the idea of immune surveillance. Immunotherapy, also named biologic therapy, represents a type of cancer treatment that boosts the body's natural defenses to fight cancer. It uses substances made by the body or in a laboratory to improve or restore immune system function. The aim of this paper is to perform a global sensitivity analysis applied to a mathematical model for the tumor-immune interaction. Global sensitivity analysis quantifies the importance of model inputs and their interactions with respect to model output. It provides an overall view on the influence of inputs on outputs as opposed to a local view of partial derivatives as in local sensitivity analysis. The model under investigation is specialized for autologous dendritic cell transfection therapy. It consists of a system of five nonlinear ordinary differential equations which define the rates of change for the following key immune cell populations: the tumor-specific CD4 T helper cells, the tumor-specific CD8 T cells or CTLs cytotoxic cells, the cancer cells that expose the tumor-associated antigens or TAAs, the mature dendritic cells loaded with the TAAs, and the IL-2 secreted by the tumor-specific CD4 T helper cells and responsible for T cell growth. We show how to globally analyze the sensitivity of this complex system by means of several graphical objects: sensitivity heat map, singular spectrum plot, and parameter sensitivity spectrum.
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Perica, Karlo, Joan G. Bieler, Andrés De León Medero, Yen-Ling Chiu, Malarvizhi Durai, Michaela Niemöller, Mario Assenmacher, Anne Richter, Mathias Oelke, and Jonathan Schneck. "Abstract 4531: Nanoscale Artificial Antigen Presenting Cells for T Cell Immunotherapy." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4531.

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Chen, Hsiu-hung, and Dayong Gao. "Quantitative Measurements of Cryobiological Characteristics of Mouse Dendritic Cells and Its Evaluation Using Commercialized Coulter Counter." In ASME 2009 4th Frontiers in Biomedical Devices Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/biomed2009-83067.

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Quantitative measurements of cell osmotic behavior and membrane transport properties is critical for the development of cell-type-specific, optimal cryopreservation conditions. A microfluidic perfusion system has been developed here to measure the kinetic changes of cell volume under various extracellular conditions, in order to determine cell osmotic behavior and membrane transport properties. The system is fabricated using soft lithographic techniques and is composed of inlets, outlets, micchannels and a perfusion chamber for trapping cells. In this study Dendritic cells (DCs) are using as a model to validate our microfluidic system with a commercialized Beckham Coulter Counter (Multisizer 3). DCs are antigen presenting cells that have been increasingly used in immunotherapy for the treatment of various diseases. Cryopreservation and banking of DCs is critical to facilitate flexible and effective immunotherapy treatment. Using mouse DCs (MDC), membrane transport properties were first investigated using our microfluidic perfusion system. Cells in the microfluidic system were perfused with 3x phosphate buffer solution. The kinetics of cell volume changes under the specific extracellular conditions were monitored by a digital camera and analyzed using a biophysical model to determine water and cryoprotectant transport properties of the cell membrane. DCs were later tested using Beckman Coulter Counter, where the kinetic osmotic behaviors of cells were quantified through the correlation between electric pulses and their corresponding cell sizes. It was shown from this study that the cryobiological characteristics of DCs determined using microfluidic perfusion system and Coulter Counter agreed well.
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Thielemans, Kris. "Abstract B36: mRNA and dendritic cell based immunotherapy." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b36.

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Luo, Danhua. "Chimeric Antigen Receptor T-Cell Immunotherapy for Cancer." In BIBE2020: The Fourth International Conference on Biological Information and Biomedical Engineering. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3403782.3403802.

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Schmidl, C., D. Riegel, E. Romero-Fernández, M. Simon, A. Adenugba, K. Singer, R. Mayr, et al. "P02.09 Integrated single-cell profiling dissects cell-state-specific enhancer landscapes of human tumor-infiltrating T cells." In iTOC9 – 9th Immunotherapy of Cancer Conference, September 22–24, 2022 – Munich, Germany. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-itoc9.28.

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Miao, Yuxuan Phoenix, Cynthia Truong, and Elaine Fuchs. "Abstract NG13: Decoding the stem cells-immune cell dialogues for cancer immunotherapy." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-ng13.

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Xu, Yuexin, Alicia J. Morales, Andrea M. H. Towlerton, Edus H. Warren, and Scott S. Tykodi. "Abstract A36: Single-cell characterization of tumor-infiltrating T cells from renal cell carcinoma." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a36.

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Bahavar, Cody F., Feifan Zhou, Aamr M. Hasanjee, Elivia Layton, Anh Lam, Wei R. Chen, and Melville B. Vaughan. "The effects of laser immunotherapy on cancer cell migration." In SPIE BiOS, edited by Wei R. Chen. SPIE, 2016. http://dx.doi.org/10.1117/12.2216592.

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Jensen, Michael. "Abstract IA22: Advanced T cell engineering for cancer immunotherapy." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-ia22.

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Reports on the topic "Cell Immunotherapy"

1

Mathis, James M. Dendritic Cell-Based Genetic Immunotherapy for Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada491946.

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Mathis, James M. Dendritic Cell-Based Genetic Immunotherapy for Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada518244.

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Mathis, James M. Dendritic Cell-Based Genetic Immunotherapy for Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada462730.

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Gilboa, Eli. Immunotherapy of Breast with Tumor RNA Transfected Dendritic Cell Vaccines. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada398155.

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Baar, Joseph. Dendritic Cell-Based Immunotherapy of Breast Cancer: Modulation by CpG. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada431640.

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Emily Morton, Emily Morton. T Cell Vaccines as an Immunotherapy for Type 1 Diabetes. Experiment, January 2015. http://dx.doi.org/10.18258/4443.

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Baar, Joseph. Dendritic Cell-Based Immunotherapy of Breast Cancer: Modulation by CpG DNA. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412155.

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Beuneu, Helene, Sandra Demaria, and Michael Dustin. Visualizing Breast Cancer Cell Interaction with Tumor-Infiltrating Lymphocytes During Immunotherapy. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada577265.

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Brink, Marcel van den. Immunotherapy of Prostate Cancer With Genetically Enhanced Tumor-Specific T-Cell Precursors. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada549122.

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Cooper, Laurence, and Rita Young. Development of Augmented Leukemia/Lymphoma-Specific T-Cell Immunotherapy for Deployment with Haploidentical, Hematompoietic Progenitor-Cell Transplant. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada487262.

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