Relevant bibliographies by topics / Immunosuppressive cells

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Immunosuppressive cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Immunosuppressive cells"

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Salminen, Antero. "Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases." Journal of Molecular Medicine 99, no. 1 (October 6, 2020): 1–20. http://dx.doi.org/10.1007/s00109-020-01988-7.

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Abstract Chronic low-grade inflammation is a common hallmark of the aging process and many age-related diseases. There is substantial evidence that persistent inflammation is associated with a compensatory anti-inflammatory response which prevents excessive tissue damage. Interestingly, the inflammatory state encountered with aging, called inflammaging, is associated with the anti-inflammaging process. The age-related activation of immunosuppressive network includes an increase in the numbers of myeloid-derived suppressor cells (MDSC), regulatory T cells (Treg), and macrophages (Mreg/M2c). Immunosuppressive cells secrete several anti-inflammatory cytokines, e.g., TGF-β and IL-10, as well as reactive oxygen and nitrogen species (ROS/RNS). Moreover, immunosuppressive cells suppress the function of effector immune cells by catabolizing l-arginine and tryptophan through the activation of arginase 1 (ARG1) and indoleamine 2,3-dioxygenase (IDO), respectively. Unfortunately, the immunosuppressive armament also induces harmful bystander effects in neighboring cells by impairing host tissue homeostasis. For instance, TGF-β signaling can trigger many age-related degenerative changes, e.g., cellular senescence, fibrosis, osteoporosis, muscle atrophy, and the degeneration of the extracellular matrix. In addition, changes in the levels of ROS, RNS, and the metabolites of the kynurenine pathway can impair tissue homeostasis. This review will examine in detail the harmful effects of the immunosuppressive cells on host tissues. It seems that this age-related immunosuppression prevents inflammatory damage but promotes the tissue degeneration associated with aging and age-related diseases. Key messages • Low-grade inflammation is associated with the aging process and age-related diseases. • Persistent inflammation activates compensatory immunosuppression with aging. • The numbers of immunosuppressive cells increase with aging and age-related diseases. • Immunosuppressive mechanisms evoke harmful bystander effects in host tissues. • Immunosuppression promotes tissue degeneration with aging and age-related diseases.
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Himes, Benjamin T., Timothy E. Peterson, Tristan de Mooij, Luz M. Cumba Garcia, Mi-Yeon Jung, Sarah Uhm, David Yan, et al. "The role of extracellular vesicles and PD-L1 in glioblastoma-mediated immunosuppressive monocyte induction." Neuro-Oncology 22, no. 7 (February 21, 2020): 967–78. http://dx.doi.org/10.1093/neuonc/noaa029.

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Abstract Background Immunosuppression in glioblastoma (GBM) is an obstacle to effective immunotherapy. GBM-derived immunosuppressive monocytes are central to this. Programmed cell death ligand 1 (PD-L1) is an immune checkpoint molecule, expressed by GBM cells and GBM extracellular vesicles (EVs). We sought to determine the role of EV-associated PD-L1 in the formation of immunosuppressive monocytes. Methods Monocytes collected from healthy donors were conditioned with GBM-derived EVs to induce the formation of immunosuppressive monocytes, which were quantified via flow cytometry. Donor-matched T cells were subsequently co-cultured with EV-conditioned monocytes in order to assess effects on T-cell proliferation. PD-L1 constitutive overexpression or short hairpin RNA–mediated knockdown was used to determined the role of altered PD-L1 expression. Results GBM EVs interact with both T cells and monocytes but do not directly inhibit T-cell activation. However, GBM EVs induce immunosuppressive monocytes, including myeloid-derived suppressor cells (MDSCs) and nonclassical monocytes (NCMs). MDSCs and NCMs inhibit T-cell proliferation in vitro and are found within GBM in situ. EV PD-L1 expression induces NCMs but not MDSCs, and does not affect EV-conditioned monocytes T-cell inhibition. Conclusion These findings indicate that GBM EV-mediated immunosuppression occurs through induction of immunosuppressive monocytes rather than direct T-cell inhibition and that, while PD-L1 expression is important for the induction of specific immunosuppressive monocyte populations, immunosuppressive signaling mechanisms through EVs are complex and not limited to PD-L1.
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Himes, Benjamin, Timothy Peterson, Jasmine Tyson, Helen Lee, Tristan deMooij, Luz Cumba-Garcia, Mi-Yeon Jung, et al. "IMMU-36. THE ROLE OF PD-L1 IN GLIOBLASTOMA-DERIVED EXTRACELLULAR VESICLES IN THE INDUCTION OF IMMUNOSUPPRESSIVE MONOCYTES." Neuro-Oncology 21, Supplement_6 (November 2019): vi126—vi127. http://dx.doi.org/10.1093/neuonc/noz175.528.

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Abstract Glioblastoma (GBM) is the most common and lethal primary brain tumor, and novel therapeutic strategies that make a substantial impact on outcomes are sorely needed. Immunotherapies have shown great promise in the treatment of a number of cancers in recent year, and a concerted effort is being made to apply these treatment paradigms to GBM. However, many GBM patients exhibit profound immunosuppression, likely limiting the efficacy of such approaches. The mechanisms of this immunosuppression are poorly understood, but tumor-derived extracellular vesicles (EVs), may play a role. We demonstrate that GBM-derived EVs induce the development of myeloid-derived suppressor cells (MDSCs) and non-classical monocytes (NCMs). We further demonstrate that these EV-induced monocytic cells are immunosuppressive, resulting in impaired T cell proliferation upon co-culture. We found that the immunosuppressive effects of tumor-derived EVs appear to be driven by the induction of these immunosuppressive monocytes, as EV treatment of T cells did not significantly impact T cell proliferation. Further, we sought to characterize the important of programmed death ligand 1 (PD-L1) in the induction of these immunosuppressive monocyte populations. We found PD-L1 to be expressed in the EVs from GBM cell lines, and that modulation in PD-L1 expression via either constitutive overexpression or shRNA-mediated knockdown resulted in concordant changes in expression in tumor-derived EVs. We demonstrate that PD-L1 is important for the induction of NCM but not for MDSCs. Taken together, these findings point to a significant role for tumor-derived EVs in the induction of immunosuppressive monocytes in GBM, and that these cells may be a driving force of systemic immunosuppression. PD-L1 is one factor expressed in EVs that has immunomodulatory properties, but additional EV cargo likely plays a major role in the induction of immunosuppressive cells.
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Díaz-Tejedor, Andrea, Mauro Lorenzo-Mohamed, Noemí Puig, Ramón García-Sanz, María-Victoria Mateos, Mercedes Garayoa, and Teresa Paíno. "Immune System Alterations in Multiple Myeloma: Molecular Mechanisms and Therapeutic Strategies to Reverse Immunosuppression." Cancers 13, no. 6 (March 17, 2021): 1353. http://dx.doi.org/10.3390/cancers13061353.

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Immunosuppression is a common feature of multiple myeloma (MM) patients and has been associated with disease evolution from its precursor stages. MM cells promote immunosuppressive effects due to both the secretion of soluble factors, which inhibit the function of immune effector cells, and the recruitment of immunosuppressive populations. Alterations in the expression of surface molecules are also responsible for immunosuppression. In this scenario, immunotherapy, as is the case of immunotherapeutic monoclonal antibodies (mAbs), aims to boost the immune system against tumor cells. In fact, mAbs exert part of their cytotoxic effects through different cellular and soluble immune components and, therefore, patients’ immunosuppressive status could reduce their efficacy. Here, we will expose the alterations observed in symptomatic MM, as compared to its precursor stages and healthy subjects, in the main immune populations, especially the inhibition of effector cells and the activation of immunosuppressive populations. Additionally, we will revise the mechanisms responsible for all these alterations, including the interplay between MM cells and immune cells and the interactions among immune cells themselves. We will also summarize the main mechanisms of action of the four mAbs approved so far for the treatment of MM. Finally, we will discuss the potential immune-stimulating effects of non-immunotherapeutic drugs, which could enhance the efficacy of immunotherapeutic treatments.
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Miyazaki, Tsubasa, Eiichi Ishikawa, Narushi Sugii, and Masahide Matsuda. "Therapeutic Strategies for Overcoming Immunotherapy Resistance Mediated by Immunosuppressive Factors of the Glioblastoma Microenvironment." Cancers 12, no. 7 (July 19, 2020): 1960. http://dx.doi.org/10.3390/cancers12071960.

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Various mechanisms of treatment resistance have been reported for glioblastoma (GBM) and other tumors. Resistance to immunotherapy in GBM patients may be caused by acquisition of immunosuppressive ability by tumor cells and an altered tumor microenvironment. Although novel strategies using an immune-checkpoint inhibitor (ICI), such as anti-programmed cell death-1 antibody, have been clinically proven to be effective in many types of malignant tumors, such strategies may be insufficient to prevent regrowth in recurrent GBM. The main cause of GBM recurrence may be the existence of an immunosuppressive tumor microenvironment involving immunosuppressive cytokines, extracellular vesicles, chemokines produced by glioma and glioma-initiating cells, immunosuppressive cells, etc. Among these, recent research has paid attention to various immunosuppressive cells—including M2-type macrophages and myeloid-derived suppressor cells—that cause immunosuppression in GBM microenvironments. Here, we review the epidemiological features, tumor immune microenvironment, and associations between the expression of immune checkpoint molecules and the prognosis of GBM. We also reviewed various ongoing or future immunotherapies for GBM. Various strategies, such as a combination of ICI therapies, might overcome these immunosuppressive mechanisms in the GBM microenvironment.
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Wang, Xiaojie, Daniel L. Metzger, Mark Meloche, Jianqiang Hao, Ziliang Ao, and Garth L. Warnock. "Generation of Transplantable Beta Cells for Patient-Specific Cell Therapy." International Journal of Endocrinology 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/414812.

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Islet cell transplantation offers a potential cure for type 1 diabetes, but it is challenged by insufficient donor tissue and side effects of current immunosuppressive drugs. Therefore, alternative sources of insulin-producing cells and isletfriendly immunosuppression are required to increase the efficiency and safety of this procedure. Beta cells can be transdifferentiated from precursors or another heterologous (non-beta-cell) source. Recent advances in beta cell regeneration from somatic cells such as fibroblasts could circumvent the usage of immunosuppressive drugs. Therefore, generation of patient-specific beta cells provides the potential of an evolutionary treatment for patients with diabetes.
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Kleist, Christian, Flavius Sandra-Petrescu, Lucian Jiga, Laura Dittmar, Elisabeth Mohr, Johann Greil, Walter Mier, et al. "Generation of suppressive blood cells for control of allograft rejection." Clinical Science 128, no. 9 (February 11, 2015): 593–607. http://dx.doi.org/10.1042/cs20140258.

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Immunosuppressants, used to prevent organ rejection, cause serious side effects. We induced specific immunosuppression towards the foreign transplant by administration of mitomycin C (MMC)-treated blood cells (MICs) from the organ donor, thus circumventing additional immunosuppressive medication.
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Morimoto-Ito, Hiroe, Masako Mizuno-Kamiya, Naoki Umemura, Yoshinori Inagaki, Eiji Takayama, Harumi Kawaki, Yasunori Muramatsu, Shinichiro Sumitomo, and Nobuo Kondoh. "Immunosuppressive Effect of Mesenchymal Stromal Cells is Enhanced by IL-1α from Oral Squamous Cell Carcinoma Cells." Open Dentistry Journal 13, no. 1 (June 30, 2019): 221–27. http://dx.doi.org/10.2174/1874210601913010221.

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Background: We have already reported that mouse Oral Squamous Carcinoma Cells (OSCCs) Sq-1979 specifically enhance the immunosuppressive activity of mesenchymal 10T1/2 cells via the functional soluble factor (s). Objective: In this report, we attempted to identify soluble factor(s) mediating the immunosuppression of Sq-1979 cells. Methods: L5-11 cells are a variant established from the metastatic lymph nodes of Sq-1979-implanted mice. Unlike parental Sq-1979 cells, however, L5-11 cells lack promotion of immunosuppressive activity in 10T1/2 cells. In order to identify cytokine mRNAs specifically expressed in Sq-1979 cells but not in L5-11 cells, cDNA microarray was performed. Conditioned medium from Sq-1979 cells (CM) was absorbed by several different neutralizing antibodies (abs) against the corresponding cytokines. The absorbed CM was then co-cultured with 10T1/2 cells and anti-CD3 antibody-stimulated mouse spleen cells. The Interferon (IFN) -γ producing capability of the stimulated spleen cells was evaluated using Enzyme-Linked Immunosorbent Assay (ELISA). By using a specific cytokine product instead of CM in this co-culture system the source of the immunosuppressive effect was identified. Results: The expression of Ccl2, Ccl7, Il1-α, IL1f6 and Il6 mRNAs was specifically elevated in Sq-1979 cells compared to L5-11 cells. The suppression of the IFN-γ producing capability of stimulated spleen cells in the co-culture system was specifically alleviated by absorbing the CM with anti-IL-1α ab. We further demonstrated that the immunosuppressive effect of CM in the co-culture system could be completely substituted by IL-1α protein (50 pmol/ ml). Conclusion: The immunosuppressive function of 10T1/2 cells is specifically promoted by IL-1α, secreted by Sq-1979 cells.
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Voll, Reinhard E., Martin Herrmann, Edith A. Roth, Christian Stach, Joachim R. Kalden, and Irute Girkontaite. "Immunosuppressive effects of apoptotic cells." Nature 390, no. 6658 (November 1997): 350–51. http://dx.doi.org/10.1038/37022.

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Pavlath, G. K., T. A. Rando, and H. M. Blau. "Transient immunosuppressive treatment leads to long-term retention of allogeneic myoblasts in hybrid myofibers." Journal of Cell Biology 127, no. 6 (December 15, 1994): 1923–32. http://dx.doi.org/10.1083/jcb.127.6.1923.

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Normal and genetically engineered skeletal muscle cells (myoblasts) show promise as drug delivery vehicles and as therapeutic agents for treating muscle degeneration in muscular dystrophies. A limitation is the immune response of the host to the transplanted cells. Allogeneic myoblasts are rapidly rejected unless immunosuppressants are administered. However, continuous immunosuppression is associated with significant toxic side effects. Here we test whether immunosuppressive treatment, administered only transiently after allogeneic myoblast transplantation, allows the long-term survival of the transplanted cells in mice. Two immunosuppressive treatments with different modes of action were used: (a) cyclosporine A (CSA); and (b) monoclonal antibodies to intracellular adhesion molecule-1 and leukocyte function-associated molecule-1. The use of myoblasts genetically engineered to express beta-galactosidase allowed quantitation of the survival of allogeneic myoblasts at different times after cessation of the immunosuppressive treatments. Without host immunosuppression, allogeneic myoblasts were rejected from all host strains tested, although the relative time course differed as expected for low and high responder strains. The allogeneic myoblasts initially fused with host myofibers, but these hybrid cells were later destroyed by the massive immunological response of the host. However, transient immunosuppressive treatment prevented the hybrid myofiber destruction and led to their long-term retention. Even four months after the cessation of treatment, the hybrid myofibers persisted and no inflammatory infiltrate was present in the tissue. Such long-term survival indicates that transient immunosuppression may greatly increase the utility of myoblast transplantation as a therapeutic approach to the treatment of muscle and nonmuscle disease.
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Dissertations / Theses on the topic "Immunosuppressive cells"

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Hamilton, Melisa June. "Immunosuppressive myeloid cells under normal and neoplastic conditions." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/39661.

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Although the importance of immunomodulatory myeloid cells in both normal physiology and carcinogenesis is well established, many questions remain regarding the specific roles and regulation of these cells. In this thesis, we explore the immunosuppressive features of macrophages [Mφs] and elucidate the mechanisms by which they suppress T cell proliferation/activation, the factors that regulate their suppressive properties, the relative potency of macrophage suppression compared to other myeloid cells, such as myeloid-derived suppressor cells (MDSCs), and the role these cells play in promoting tumor growth and metastasis. We demonstrate herein that in response to interferon (IFN)-beta, which is secreted by activated T cells, resident macrophages from non-tumor-bearing mice acquire immunosuppressive properties that are mediated by nitric oxide (NO). Moreover, our data reveal a novel role for Toll-like receptor (TLR)-induced IFN-beta in regulating the immunosuppressive properties of macrophages. We also demonstrate for the first time that in vitro culture conditions profoundly affect the immunosuppressive functions of MDSCs. Specifically, we show that serum antagonizes the suppressive abilities of MDSCs from 4T1 tumor-bearing mice and that the major serum protein albumin mediates these effects, in part by reducing reactive oxygen species (ROS) production from MDSCs. These findings have important implications, since the accurate detection and quantification of immunosuppression is critical for both the identification and functional analysis of tumor-induced MDSCs. We also explore the phenotypic and functional heterogeneity of tumor-induced myeloid cells and compare the immunosuppressive functions of different populations isolated from normal and tumor-bearing mice. We show that tumors that induce the accumulation of myeloid cells also enhance the suppressive functions of these cells. In addition, we demonstrate that, in vitro, tumor-induced macrophages are significantly more potent immune suppressors than tumor-induced MDSCs on a per cell basis, and suppress T cell responses via distinct mechanisms. Finally, we present data showing that treating metastatic mammary tumor-bearing mice with all-trans-retinoic acid (ATRA) decreases MDSCs, increases macrophages, and enhances metastatic growth. Taken together, these findings advance our understanding of the factors that regulate myeloid cell functions in normal and neoplastic tissues and may lead to improved immunotherapies to treat human disease.
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Alves, Inês Sofia Moutinho. "Contribution of ER stress to tumor immunosuppressive microenvironment." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/14290.

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Mestrado em Bioquímica - Bioquímica Clínica
Breast cancer is the most prevalent cancer among women and also one of the oncologic pathologies that causes more deaths. In the last decades several studies have reported that solid tumors generate an immunosuppressive microenvironment. This microenvironment (acidosis, hypoxia, glucose deprivation and cytokines) is favourable to endoplasmic reticulum (ER) stress induction. ER stress is primarily a response towards the re-establishment of homeostasis; however if not resolved it usually results in cell death by apoptosis. Nevertheless, ER stress and unfolded protein response (UPR) play a paradoxical role in cancer physiopathology: the three branches of UPR, PERK, IRE1 and ATF6 actively contribute to signalling of survival and metastasis mechanisms. Recently it was reported a possible transmission of ER stress from tumor cells to immune cells, modulating the phenotype and function of recipient cells. Thus, the aim of the present work is to assess the ability and the respective mechanisms by which T-47D tumor cells transmit ER stress to THP-1 monocytes, and the consequences of this transmission. ER stress transmission was only observed when pharmacological ER stress inducers were used, such as tunicamycin, contrarily to physiological stimulation, as glucose deprivation. Additionally, it was found that tunicamycin seems to be transported within exosomes which, in turn, directly induces ER stress on monocytes. It was also observed that exosomes derived from glucose deprived T-47D cells do not transmit ER stress; however these exosomes conduct monocytes towards a particular proinflammatory profile, accompanied by the decrease of its maturation status. Overall, our results question the ER stress mechanism originally described, showing that pharmacological ER stress inducers can be transported within exosomes and directly inducing ER stress on recipient cells.
O cancro da mama é o cancro de maior incidência entre as mulheres, sendo também uma das situações oncológicas que mais mortes causa. Na última década inúmeros estudos têm demonstrado que os tumores sólidos geram um microambiente favorável à evasão/subversão do sistema imune. Esse microambiente (acidose, hipoxia, deprivação de glucose, citoquinas) é muita das vezes propicio à indução de stress do reticulo endoplasmático (RE). O stress do RE é primariamente uma resposta no sentido de restabelecer a homeostasia no entanto se não resolvido resulta normalmente na morte celular por apoptose. O stress do RE e a respetiva resposta às proteínas mal conformadas (UPR), desempenham um papel paradoxal na fisiopatologia do cancro: os três ramos da UPR, PERK, IRE1 e ATF6, contribuem ativamente para a sinalização de alguns mecanismos de sobrevivência e metastização. Recentemente, foi descrita uma possível transmissão do stress do RE das células tumorais para as células do sistema imunitário, modulando a ação destas. Desta forma, pretendeu avaliar-se com o presente trabalho a capacidade e os mecanismos pelos quais células tumorais T-47D transmitem o stress do RE para células monocíticas THP-1, e quais as consequências desta transmissão. A transmissão foi apenas observada aquando da utilização de indutores farmacológicos como a tunicamicina, não se registando para estímulos fisiológicos como a deprivação de glucose. Por outro lado, verificou-se que a tunicamicina parece ser transportada via exossomas e desta forma induzir diretamente stress do RE nos monócitos. Observou-se ainda que os exossomas provenientes das células T-47D em stress do RE por deprivação de glucose apesar de não transmitirem o referido stress conduzem os monócitos para um perfil pró-inflamatório específico diminuindo ainda a sua capacidade de maturação. Em geral, os nossos resultados questionam seriamente o mecanismo de transmissão de stress ER tal como originalmente descrito, mostrando que no uso de indutores farmacológicos o que parece ocorrer é o transporte do fármaco em vesículas e a indução direta nas células recetoras.
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Glennie, Sarah Jane. "The molecular mechanisms mediating the immunosuppressive effects of mesenchymal stem cells." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417349.

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Khanolkar, Rahul Chaitanya. "Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=202767.

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The leukocyte immunoglobulin like receptors (LILRs) are a group of receptors with immunomodulatory effects. Group 1 LILRs comprise of LILRB1, among others, and bind to class 1 MHC molecules and transmits inhibitory signals. Studies have shown that LILRB1 ligation during the monocyte differentiation process into dendritic cells (DCs) results in the generation of a population of cells that are tolerogenic. Here we hypothesize that this tolerogenic nature of the resultant cells is due to the high expression of nuclear factor kappa – light chain enhancer of activated B cells (NF-κB) inhibitor – A20 binding inhibitor of NF-κB signalling 1 (ABIN1). In this study we analyzed the effect that ABIN1 exerts on the maturation of DCs and CD14+HLA-DRlow/- monocytes - a population of cells that have been recently been identified as myeloid derived suppressor cells (MDSCs) in humans. LILRB1 ligated DCs and CD14+HLA-DRlow/- monocytes, when treated with ABIN1 siRNA, displayed an increase in the expression of antigen presentation and co-stimulatory molecules such as CD80, CD86, HLA-DR and HLA-ABC and displayed a greater capacity to produce cytokines like IL-12 and IFN-α. Additionally, they displayed a greater capacity to stimulate the adaptive component of the immune system in terms of IFN-γ production, cell proliferation and adapter molecule and mitogen activated protein kinase (MAPK) activation in T cells. Based on the results we obtained, it can be concluded that ABIN1 plays a significant role in maintaining the immature and suppressive phenotype of immature myeloid cells (IMCs) by dampening NF-κB signalling, while also exerting a negative effect on antiviral signalling.
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Delaney, Michael Paul. "Immunosuppressive drug interactions and resistance in mononuclear cells from renal transplant patients." Thesis, University of Warwick, 2001. http://wrap.warwick.ac.uk/3703/.

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Existing anti-rejection drug regimes are inadequate since patients receive drugs despite serious side effects and poor response. New drugs are being developed which ultimately may allow for prescribing of rational, patient-specific immunosuppressive drug protocols. During this thesis the investigation of lymphocyte responses from renal transplant recipients to the immunosuppressant drugs Cyclosporin A (Cy A), FK506 and SDZ RAD were explored to understand the variation in sensitivity of lymphocytes to Cy A and FK506, the development of drug resistance, including resistance mechanisms, and the interactions between FK506 and SDZ RAD. Cy A and FK506 are substrates for P-glycoprotein (P-gp), the product of the multidrug-resistance (MDR1) gene in man. A hypothesis established during this thesis was that P-gp dependent mechanisms explain variations in lymphocyte sensitivities to Cy A and FK50. Lymphocytes from renal transplant recipients were assessed for their sensitivity to Cy A and FK506 and subsequently for P-gp expression and functional activity by flow cytometry. In further lymphocyte cultures the effect of the specific P-gp inhibitor, PSC 833 on sensitivity was investigated. Finally, the effects of the combination of FK506 and SDZ RAD in lymphocyte cultures were analysed. Results demonstrate a wide range in lymphocyte sensitivity to both Cy A and FK506, with the development of selective resistance to the drug used for treatment. All patients demonstrated P-gp functional activity but P-gp expression was not demonstrable. P-gp function did not account for the variation in lymphocyte sensitivity. There was no evidence of antagonism of effect of SDZ RAD in combination with FK506. In conclusion, these results suggest that non-P-gp mechanisms account for variations in lymphocyte sensitivity to Cy A and FK506. Combination therapy with SDZ RAD and FK506 is unlikely to be antagonistic in future treatment protocols.
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Duque, Marta. "The immunosuppressive potential of human amniotic membrane extract." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15498.

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Mestrado em Bioquímica - Bioquímica Clínica
Both mesenchymal stromal cells (MSCs) and human amniotic membrane (hAM) possess immunoregulatory potential, driving several studies to focus on their application in the prevention and treatment of immunological disorders, and especially on their ability to modulate T cell responses. However there is little information regarding the concrete effects over different activation and differentiation stages of T cells. The main objective of this study was to determine whether or not a hAM extract (hAME) had a differential effect over different T cell subpopulations (CD4+ and CD8+ T naïve, central memory, effector memory and effector cells). Thus, peripheral blood mononuclear cells (PBMC) were cultured in the presence or absence of hAME and stimulated with phorbol myristate acetate (PMA) plus ionomycin. Cell proliferation was evaluated through a thymidine incorporation assay and the percentages of pro-inflammatory cytokine producing T cells were determined by flow cytometry. The phenotype of hAM-derived cells was also assessed by flow cytometry. Plus, the mRNA expression of selected genes was evaluated in purified CD4+ and CD8+ T cells, regulatory T cells (Treg) and γδ T cells. The hAM-derived cells contained hAM epithelial cells and MSCs. The extract displayed an antiproliferative effect and reduced the frequency of tumor necrosis factor-alpha (TNFα), interferon gamma (IFNγ), and interleukin-2 (IL-2) producing cells, within all T cell subsets. The hAME also diminished the frequency of IL-17 and IL-9 producing T cells. The pattern of inhibition varied between CD4+ and CD8+ T cells, between T cell subsets, and depending on the cytokine under study. The hAME also produced a decrease in mRNA expression of granzime B, perforin and activating receptor NKG2D by CD8+ T cells, γδ T cells as well as an upregulation of Foxp3 and IL-10 gene expression in CD4+ T cells and an upregulation of IL-10 mRNA expression in Treg cells. These results show that the hAME differentially regulates different T cell subsets and therefore the effect of the hAME over T cells responses will depend on the T cell subpopulations involved. Still, the hAME has an overall antiinflammatory action.
Tanto as células mesenquimais do estroma (MSCs) como a membrana amniótica humana (hAM) possuem capacidade imunoreguladora, levando a que vários estudos se debrucem sobre a sua aplicação na prevenção e tratamento de doenças imunológicas, e especialmente sobre a sua capacidade de modular células T. No entanto, há pouca informação acerca dos efeitos concretos sobre diferentes fases de ativação e diferenciação de células T. O principal objetivo deste estudo foi determinar se um extrato de hAM (hAME) exerce efeito diferencial sobre diferentes subpopulações de células T (células T CD4+ e CD8+ naïve, memória central, memória efetoras e efetoras). Para esse efeito, células mononucleares do sangue periférico (PBMC) foram cultivadas na presença ou ausência de hAME e estimuladas com acetato miristato de forbol (PMA) mais ionomicina. A proliferação celular foi avaliada por um ensaio de incorporação de timidina e as percentagens de linfócitos T produtores de citocinas pró-inflamatórias foram determinadas por citometria de fluxo. O fenótipo de células derivadas de hAM foi também determinado por citometria de fluxo. Foi ainda estudada a expressão de mRNA em células T CD4+ e CD8+, células T reguladoras (Treg) e células T γδ purificadas. As células derivadas de hAM continham células epiteliais e MSCs. O extrato exibiu um efeito anti-proliferativo e reduziu a frequência de células produtoras de fator de necrose tumoral alfa (TNFα), interferão gama (IFNγ), e interleucina-2 (IL-2) em todas as subpopulações de células T estudadas, assim como a frequência de células T produtoras de IL-17 e IL-9. O padrão de inibição variou entre células T CD4+ e CD8+, entre cada subpopulação celular, e dependendo da citocina em estudo. O hAME provovou também diminuição da expressão de mRNA de granzima B, perforina e recetor de ativação NKG2D em células T CD8+e células T γδ, assim como o aumento de expressão de Foxp3 e IL-10 em células T CD4+, e aumento de expressão IL-10 em células Treg. O hAME regula diferencialmente diferentes subpopulações de células T e, portanto, o efeito do hAME sobre respostas de células T será dependente das subpopulações de células T envolvidas, ainda assim, hAME tem uma ação global anti-inflamatória.
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Nurmenniemi, P. (Petri). "Inflammatory cells and mitotic activity of keratinocytes in gingival overgrowth induced by immunosuppressive- and nifedipine medication." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514279964.

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Abstract Both immunosuppressive and nifedipine medication have been associated with drug-induced gingival overgrowth. There are several hypothetical mechanisms for drug-induced gingival overgrowth, such as the influence of genetic predisposition, alterations in gingival tissue homeostasis, especially in the function of fibroblasts, and drug-induced action on growth factors. Clinical studies have also shown that, those with poor oral hygiene status drug-induced gingival overgrowth is more prevalent and severe than those with good oral hygiene status. The working hypothesis was that immunosuppressive medication and/or nifedipine medication affects inflammatory cell profile and mitotic activity of keratinocytes in human overgrown gingiva. We studied gingival samples, collected from nifedipine-medicated cardiac outpatients and immunosuppression-medicated organ-transplant recipients. Patients were placed into four groups: 1) the immunosuppression group, patients receiving cyclosporin-A (CsA), azathioprine (AZA) and prednisolone (Pred) 2) the immunosuppression plus nifedipine group, patients receiving CsA, AZA, Pred. and nifedipine 3) the nifedipine group patients receiving only nifedipine and 4) the non-medicated control group. All of the samples related to moderate to severe degrees of gingival overgrowth, covering half to two thirds of the clinical crown. The aim of the study was to investigate the occurrence of Langerhans cells, macrophages, mast cells and mitotic activity of keratinocytes in human drug-induced overgrown gingiva, and consequently to assess their possible role in the pathogenesis of drug-induced gingival overgrowth. We found that immunosuppressive medication increased the numbers of reparative macrophages (RM3/1) and decreased the numbers of tryptase- and chymase-positive mast cells (MCTC) cells. We have also shown that immunosuppressive and nifedipine medication decreased the numbers of Langerhans cells (CD1a) and increased the numbers of 27E10-macrophages parallelly. Additionally we found increase in the mitotic activity of gingival keratinocytes and even two-fold thickening of gingival epithelium in immunosuppressive and nifedipine medication-induced gingival overgrowth as compared with healthy gingiva. Immunosuppressive medication activated gingival epithelium (27E10 expression in gingival keratinocytes) more than nifedipine medication. In conclusion, our results suggest that gingival overgrowth among immunosuppressive- and nifedipine-medicated patients is related to alteration of tissue homeostasis. First, this suggestion is supported by changes found in the numbers of cells that directly affect connective tissue turnover, e.g. reparative macrophages (RM3/1) and mast cells. Changes in the numbers of these cells could alter the cytokine- and growth factor-profile, which affects fibroblast function. Secondly, we found changes in the numbers of cells involved in regulation of inflammation, e.g. Langerhans cells and monocytes as compared with healthy controls. Immunosuppressive medication could directly activate gingival keratinocytes. We suggest that our findings mainly reflect the effects of immunosuppressive medication, but the role of inflammation cannot be excluded. The changes observed above represent differences of the pathogenesis of drug-induced gingival overgrowth between immunosuppressive and nifedipine medication. It must be however remembered that drug-induced gingival overgrowth is a result of multicausal intrinsic and extrinsic factors. Age, gender, concomitant medication with multiple drugs, plaque accumulation, and genetic disposition are additional risk factors. The abnormal distribution of specific immune system cell subpopulations does not alone prove a functional relationship to gingival overgrowth.
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Freeman, Lisa. "An investigation into the regulation of immunosuppressive steroids by human monocyte-derived dendritic cells." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433428.

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Centuori, Sara Mozelle. "NEGATIVE REGULATION OF REGULATORY T CELLS BY MYELOID-DERIVED SUPPRESSOR CELLS IN CANCER." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/145099.

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Myeloid-derived suppressor cells (MDSC) and regulatory T cells (Treg) play an essential role in the immunosuppressive networks that contribute to tumor immune evasion. The mechanisms by which tumors promote the expansion and/or function of these suppressive cells and the cross-regulation between MDSC and Treg remain incompletely defined. The current work evaluates the influence of MDSC, expanded in two mouse cancer models, on immunosuppressive Treg. We demonstrate that tumor-induced MDSC endowed with the potential of suppressing conventional T lymphocytes surprisingly impair TGF-β1-mediated generation of induced Treg (iTreg) from naïve CD4⁺ T lymphocytes. Suppression of iTreg generation by MDSC occurs early in the differentiation process, and is cell contact dependent. This inhibition of FoxP3-expressing T lymphocyte differentiation by MDSC does not depend on arginase 1, cystine/cysteine depletion, iNOS/NO, or PD-1/PD-L1 signaling. These findings therefore indicate that MDSC from tumor-bearing hosts have the heretofore unreported ability to restrict some immunosuppressive Treg subpopulations.
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Ochando, Jordi Cano. "In vitro studies of the effects of fungal-derived immunosuppressive agents on MCF7 breast cancer cells and MOLT4 leukaemia cells." Thesis, De Montfort University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393220.

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Books on the topic "Immunosuppressive cells"

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Ochando, Jordi Cano. In vitro studies of the effects of fungal-derived immunosuppressive agents on MCF7 breast cancer cells and MOLT4 leukaemia cells. Leicester: De Montfort University, 2002.

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Chen, Xin, and Magdalena Plebanski, eds. The Role of TNF-TNFR2 Signal in Immunosuppressive Cells and its Therapeutic Implications. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-306-7.

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B, Vogelsang Georgia, and Pavletic Steven, eds. Chronic graft versus host disease: Interdisciplinary management. Cambridge [England] ; New York: Cambridge University Press, 2009.

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Strasfeld, Lynne. While the T Cells Were Sleeping. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199938568.003.0215.

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These case studies illustrate infections encountered in hospitals among patients with compromised immune systems. As a result of immunocompromise, the patients are vulnerable to common and uncommon infections. These cases are carefully chosen to reflect the most frequently encountered infections in the patient population, with an emphasis on illustrations and lucid presentations to explain the state-of-the-art approaches in diagnosis and treatment. Common and uncommon presentations of infections are presented while the rare ones are not emphasized. The cases are written and edited by clinicians and experts in the field. Each of these cases highlight the immune dysfunction that uniquely predisposed the patient to the specific infection, and the cases deal with infections in the cancer patient, infections in the solid organ transplant recipient, infections in the stem cell recipient, infections in patients receiving immunosuppressive drugs, and infections in patients with immunocompromise that is caused by miscellaneous conditions.
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Jean-François, Bach, ed. T-cell-directed immunointervention. Oxford [England]: Blackwell Scientific Publications, 1993.

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David, Naor, ed. Immunosuppression and human malignancy. Clifton, N.J: Humana Press, 1989.

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van der Vlag, Johan, and Jo H. M. Berden. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.
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Cerhan, James R., Claire M. Vajdic, and John J. Spinelli. The Non-Hodgkin Lymphomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0040.

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The non-Hodgkin lymphomas (NHL) are a heterogeneous group of over forty lymphoid neoplasms that have undergone a major redefinition over the last twenty-five years, in part due to advances in immunology and genetics as well as implementation of the WHO classification system. NHLs are considered clonal tumors of B-cells, T-cells, or natural killer (NK) cells arrested at various stages of differentiation, regardless of whether they present in the blood (lymphoid leukemia) or lymphoid tissues (lymphoma). In the United States, the age-standardized NHL incidence rate (per 100,000) doubled from 1973 (10.2) to 2004 (21.4) and then stabilized, while five-year relative survival rates improved from 42% in 1973 to 70% in 2004. Established risk factors for NHL or specific NHL subtypes include infectious agents (HTLV-1, HIV, EBV, HHV8, HCV, H. pylori), immune dysregulation (primary immunodeficiency, transplantation, autoimmunity, and immunosuppressive drugs), family history of lymphoma, and common genetic variants identified by genome-wide association studies.
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Kuypers, Dirk R. J., and Maarten Naesens. Immunosuppression. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0281_update_001.

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Combination immunosuppressive therapy produces excellent short-term results after kidney transplantation. Long-term graft survival has improved, but less dramatically. Death with a functioning graft remains the primary cause of graft loss. Dosing of current immunosuppressive therapy balances between careful clinical interpretation of time-driven immunological risk assessments and drug-related toxicity on the one hand, and the use of simple surrogate drug exposure indicators like blood/plasma concentrations on the other. The combined use of calcineurin-inhibitors (CNIs) with mycophenolic acids and corticosteroids has been fine-tuned over the last decade, based on empirically derived observations as well as on the results of large multicentre randomized clinical studies. Corticosteroid withdrawal and avoidance are feasible, at least in patients with a low immunological risk, but CNI-free protocols have had few long-term successes. Some minimization strategies have increased risk of developing acute rejection or (donor-specific) anti-HLA antibodies, with deleterious effects on the graft. Mammalian target of rapamycin inhibitors (mTORi) have shown limited benefit in early CNI replacement regimens and their long-term use as primary drug is hampered by intolerance. In the setting of particular malignant disease occurring after transplantation, such as squamous cell carcinoma of the skin and Kaposi’s sarcoma, mTORi seem promising. Induction agents (anti-interleukin 2 receptor monoclonal antibodies, antithymocyte globulins) effectively diminish the risk of early immunological graft loss in recipients with moderate to high immunological risk but at the price of more infectious or malignant complications. While personalized transplantation medicine is only in its early stages of development, attempts are made to quantitatively measure the clinical degree of immunosuppression, to tailor immunosuppressive therapy more specifically to the patient’s individual profile, and to monitor graft status by use of invasive (e.g. surveillance renal biopsies) and non-invasive biomarkers. These scientific endeavours are a necessity to further optimize the current immunosuppressive therapy which will remain for some time to come.
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Misbah, Siraj. Immunosuppressive therapy and therapeutic monoclonal antibodies. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0302.

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The term immunosuppressive therapy encompasses all forms of treatment that dampens function of the recipient’s immune system, with a view to controlling severe autoimmune, inflammatory, or allergic disease. The predominant targets of these agents are T-lymphocytes with multiple downstream effects, including containment of T-cell activation, inhibition of cytokine production, restriction of clonal expansion, and varying degrees of suppression of B-cell function. This chapter reviews the clinical use of monoclonal antibodies and other immunosuppressive agents, and their mechanisms of action.
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Book chapters on the topic "Immunosuppressive cells"

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Lanza, Francesco, Diana Campioni, Endri Mauro, Annalisa Pasini, and Roberta Rizzo. "Immunosuppressive Properties of Mesenchymal Stromal Cells." In Advances in Stem Cell Research, 281–301. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-940-2_15.

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Hachimura, S., T. Hisatsune, Y. Minai, and S. Kaminogawa. "Immunosuppressive Functions of Cells from Intestinal Tissues." In Animal Cell Technology: Basic & Applied Aspects, 491–97. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2844-5_66.

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Kalesnikoff, Janet, and Stephen J. Galli. "Antiinflammatory and Immunosuppressive Functions of Mast Cells." In Methods in Molecular Biology, 207–20. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-869-0_15.

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Kusmartsev, Sergei A., I. N. Kusmartseva, S. G. Afanasyev, and N. V. Cherdyntseva. "Immunosuppressive Cells in Bone Marrow of Patients with Stomach Cancer." In Advances in Experimental Medicine and Biology, 189–94. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5357-1_30.

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Park, Joshua K., Nathan J. Coffey, Aaron Limoges, and Anne Le. "The Heterogeneity of Lipid Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism, 39–56. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_3.

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AbstractThe study of cancer cell metabolism has traditionally focused on glycolysis and glutaminolysis. However, lipidomic technologies have matured considerably over the last decade and broadened our understanding of how lipid metabolism is relevant to cancer biology [1–3]. Studies now suggest that the reprogramming of cellular lipid metabolism contributes directly to malignant transformation and progression [4, 5]. For example, de novo lipid synthesis can supply proliferating tumor cells with phospholipid components that comprise the plasma and organelle membranes of new daughter cells [6, 7]. Moreover, the upregulation of mitochondrial β-oxidation can support tumor cell energetics and redox homeostasis [8], while lipid-derived messengers can regulate major signaling pathways or coordinate immunosuppressive mechanisms [9–11]. Lipid metabolism has, therefore, become implicated in a variety of oncogenic processes, including metastatic colonization, drug resistance, and cell differentiation [10, 12–16]. However, whether we can safely and effectively modulate the underlying mechanisms of lipid metabolism for cancer therapy is still an open question.
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Ford, Megan S., and Li Zhang. "The Development, Activation, Function and Mechanisms of Immunosuppressive Double Negative (DN) T Cells." In Regulatory T Cells and Clinical Application, 543–61. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-77909-6_29.

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Dazzi, Francesco, and Ilaria Marigo. "The Immunosuppressive Properties of Adult Stem Cells: Mesenchymal Stem Cells as a Case Study." In The Immunological Barriers to Regenerative Medicine, 175–97. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5480-9_10.

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Zamiri, Parisa, Sunao Sugita, and J. Wayne Streilein. "Immunosuppressive Properties of the Pigmented Epithelial Cells and the Subretinal Space." In Immune Response and the Eye, 86–93. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000099259.

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Sasso, Maria Stella, Vincenzo Bronte, and Ilaria Marigo. "Cancer Immune Modulation and Immunosuppressive Cells: Current and Future Therapeutic Approaches." In Nano-Oncologicals, 187–214. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08084-0_7.

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Kawakami, Yutaka, Tomonori Yaguchi, Hidetoshi Sumimoto, Chie Kudo-Saito, Nobuo Tsukamoto, Tomoko Iwata-Kajihara, Shoko Nakamura, et al. "Roles of Signaling Pathways in Cancer Cells and Immune Cells in Generation of Immunosuppressive Tumor-Associated Microenvironments." In The Tumor Immunoenvironment, 307–23. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6217-6_12.

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Conference papers on the topic "Immunosuppressive cells"

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Lu, Xin. "Abstract 4063: Target immunosuppressive myeloid cells to enhance cancer immunotherapy." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4063.

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Fernandez, I. E., F. R. Greiffo, V. Viteri-Alvarez, I. Bastidas, R. Roy, M. Frankenberger, J. Behr, A. Forrest, A. Hilgendorff, and O. Eickelberg. "Myeloid-Derived Suppressor Cells Orchestrate Immunosuppressive Networks in Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1231.

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Rollison, Dana E., Neil A. Fenske, Basil Cherpelis, Jane L. Messina, Yayi Zhao, Rossybelle P. Amorrortu, Rebecca Hesterberg, and Pearlie K. Epling-Burnette. "Abstract 3492: Circulating immunosuppressive regulatory T cells and risk of incident cutaneous squamous cell carcinoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3492.

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Huijts, Charlotte M., Famke L. Schneiders, Henk M. Verheul, Tanja D. de Gruijl, and Hans J. van der Vliet. "Abstract 4720: mTOR inhibition is required for conversion of invariant NKT cells into immunosuppressive regulatory cells." 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.am2013-4720.

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Chang, ZeNan L., Michael H. Lorenzini, and Yvonne Y. Chen. "Abstract IA08: Engineering T cells to resist and convert immunosuppressive tumor microenvironments." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-ia08.

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Rollison, Dana E., Shalaka S. Hampras, Jane L. Messina, Neil A. Fenske, Basil S. Cherpelis, Michael J. Schell, Rhianna Reed, et al. "Abstract 4960: Recent ultraviolet radiation exposure and circulating immunosuppressive T-regulatory cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4960.

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Long, Meixiao, Kyle A. Beckwith, Priscilla Do, Amber Gordon, Amy Lehman, Kami Maddocks, Carolyn Cheney, et al. "Abstract B041: Ibrutinib treatment counteracts the immunosuppressive activity of malignant B cells." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b041.

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Hall, SRR, L. Wang, C. Simillion, S. Berezowska, P. Dorn, RW Peng, TM Marti, and RA Schmid. "Tumor associated CD90+ mesenchymal cells are chemoresistant and immunosuppressive in human non-small cell lung cancer." In DACH-Jahrestagung Thoraxchirurgie. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1694179.

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Mirlekar, Bhalchandra, and Yuliya Pylayeva-Gupta. "Abstract PR21: IL-35+ B cells establish immunosuppressive network in pancreatic ductal adenocarcinoma." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-pr21.

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Khramtsova, Galina F., Rita Nanda, Ekaterina A. Khramtsova, Lise Sveen, Sope Olugbile, and Olufunmilayo I. Olopade. "Abstract 462: Cytotoxic CD8+ T cells and immunosuppressive T regulatory cells are associated with aggressive breast cancer subtypes." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-462.

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