Relevant bibliographies by topics / Surveillance immune

Contents

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

Academic literature on the topic 'Surveillance immune'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Surveillance immune"

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Shastri, Nilabh, Chansu Park, and Jian Guan. "Immune surveillance of immune surveillance." Molecular Immunology 150 (October 2022): 2. http://dx.doi.org/10.1016/j.molimm.2022.05.018.

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Swann, Jeremy B., and Mark J. Smyth. "Immune surveillance of tumors." Journal of Clinical Investigation 117, no. 5 (May 1, 2007): 1137–46. http://dx.doi.org/10.1172/jci31405.

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Grossman, Zvi, and Ronald B. Herberman. "‘Immune surveillance’ without immunogenicity." Immunology Today 7, no. 5 (May 1986): 128–31. http://dx.doi.org/10.1016/0167-5699(86)90075-7.

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Prehn, Richmond T., and Liisa M. Prehn. "The flip side of immune surveillance: immune dependency." Immunological Reviews 222, no. 1 (April 2008): 341–56. http://dx.doi.org/10.1111/j.1600-065x.2008.00609.x.

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Kim, Ryungsa, Manabu Emi, and Kazuaki Tanabe. "Cancer immunoediting from immune surveillance to immune escape." Immunology 121, no. 1 (May 2007): 1–14. http://dx.doi.org/10.1111/j.1365-2567.2007.02587.x.

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Schaller, Julien, and Judith Agudo. "Metastatic Colonization: Escaping Immune Surveillance." Cancers 12, no. 11 (November 16, 2020): 3385. http://dx.doi.org/10.3390/cancers12113385.

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Cancer immunotherapy has shifted the paradigm in cancer therapy by revitalizing immune responses against tumor cells. Specifically, in primary tumors cancer cells evolve in an immunosuppressive microenvironment, which protects them from immune attack. However, during tumor progression, some cancer cells leave the protective tumor mass, disseminating and seeding secondary organs. These initial disseminated tumor cells (DTCs) should potentially be susceptible to recognition by the immune system in the new host tissues. Although Natural Killer or T cells eliminate some of these DTCs, a fraction escape anti-tumor immunity and survive, thus giving rise to metastatic colonization. How DTCs interact with immune cells and the underpinnings that regulate imperfect immune responses during tumor dissemination remain poorly understood. Uncovering such mechanisms of immune evasion may contribute to the development of immunotherapy specifically targeting DTCs. Here we review current knowledge about systemic and site-specific immune-cancer crosstalk in the early steps of metastasis formation. Moreover, we highlight how conventional cancer therapies can shape the pre-metastatic niche enabling immune escape of newly arrived DTCs.
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Lowe, Scott. "Immune Surveillance of Senescent Cells." Innovation in Aging 5, Supplement_1 (December 1, 2021): 246. http://dx.doi.org/10.1093/geroni/igab046.952.

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Abstract Cellular senescence involves a stable cell cycle arrest and a secretory program that modulates the tissue environment. In cancer, senescence acts as a potent barrier to tumorigenesis and, though many cancers evade senescence during the course of tumor evolution, ionizing radiation and conventional chemotherapy can, to varying degrees, induce senescence in tumor cells leading to potent anticancer effects. Conversely, the aberrant accumulation of senescent cells can reduce regenerative capacity and lead to tissue decline, contributing to tissue pathologies associated with age or the debilitating side-effects of cancer therapy. Our laboratory studies mechanisms of cellular senescence with the ultimate goal of developing strategies to modulate senescence for therapeutic benefit. We have focused on how senescent cells trigger immune surveillance to facilitate their own elimination or, when that fails, how synthetic immune cells (i.e. CAR T cells) can be directed to eliminate senescent cells. Recent advances in understanding senescent cell surveillance by the immune system will be discussed.
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Ahmad, Aamir. "Tumor microenvironment and immune surveillance." Microenvironment and Microecology Research 4, no. 1 (2022): 6. http://dx.doi.org/10.53388/mmr2022006.

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Oh, Julia, and Derya Unutmaz. "Immune cells for microbiota surveillance." Science 366, no. 6464 (October 24, 2019): 419–20. http://dx.doi.org/10.1126/science.aaz4014.

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Zanetti, M., and N. R. Mahadevan. "Immune Surveillance from Chromosomal Chaos?" Science 337, no. 6102 (September 27, 2012): 1616–17. http://dx.doi.org/10.1126/science.1228464.

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Dissertations / Theses on the topic "Surveillance immune"

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Rosenthal, Rachel Suzanne. "Immune editing and surveillance in cancer evolution." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10047362/.

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Cancer is an evolutionary disease, reliant on genetic diversity and sculpted by selective forces from the immune microenvironment. Here, I use genomics data to decipher the tumor’s evolutionary trajectory and corresponding shifts in the immune contexture to elucidate the events governing tumor immunogenicity and the immune evasive mechanisms evolved by the tumor. To better understand the mutational processes contributing to intratumor heterogeneity in individual tumors, a method to quantify the activity of mutational processes in a single tumor sample was developed and applied to temporally dissected mutations. The clinical relevance of intratumor heterogeneity was examined in the context of immune recognition and modulation. Increased clonal neoantigen burden and minimal neoantigen intratumor heterogeneity were found to associate with improved patient outcome, both in the treatment-naïve and immunotherapy-treated setting. The identification of T-cells recognizing clonal neoantigens further supported the clinical importance of targeting neoantigens present in every cancer cell. Mechanisms of immune evasion were considered through the development of a method to identify loss-of-heterozygosity at the HLA locus, overcoming the challenges posed by the polymorphic nature of the locus. HLA loss-of-heterozygosity was found to be a frequent subclonal event in NSCLC, under strong selective pressure and associated with increased subclonal neoantigen burden. Finally, the immune microenvironment was examined through multi-region RNAseq, permitting the quantification of immune infiltration and allowing for the identification of heterogeneously immune infiltrated tumors. Supporting the interplay between genetic events and the immune contexture, a relationship between the genomic features of the tumor and immune infiltration was observed, with HLA loss-of-heterozygosity specifically identified as occurring within a highly active immune microenvironment. This thesis shows how an improved understanding of the relationship between the tumor and the immune system can illuminate features dictating immune recognition and evasion and how that knowledge may inform the development and implementation of successful immunotherapy.
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SCHEIDECKER, CATHERINE. "Cellule nk : surveillance immune et resistance naturelle." Strasbourg 1, 1987. http://www.theses.fr/1987STR10724.

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Marri, Eswari. "Immune surveillance of activated immune and tumour cells by surfactant protein D." Thesis, Brunel University, 2015. http://bura.brunel.ac.uk/handle/2438/13847.

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Surfactant protein D (SP-D) is a carbohydrate/charged pattern recognition molecule of the innate immune system. By virtue of its ability to recognize an array of carbohydrate patterns on the surface of a range of pathogens, SP-D can bring about opsonisation, enhanced phagocytosis and killing of a diverse range of viruses, bacteria and fungi. In addition to antimicrobial functions, which also includes bacteriostatic and fungistatic properties SP-D has also been shown to bind allergens derived from a number of sources including house dust mite, Aspergilllus fumigatus and pollen grains. SP-D allergen interaction leads to inhibition of specific IgE binding and subsequent downregulation of histamine release from sensitized basophils and mast cells. Thus, a number of murine models of pulmonary hypersensitivity and allergic asthma induced by ovalbumin, house dust mite and Aspergillus fumigatus allergens/antigens have been tested for the ability of SP-D to dampen allergic symptoms on the immunological parameters. In general, treatment of allergic models with a recombinant fragment of human SP-D (rh SP-D; composed of trimeric, neck and carbohydrate recognition domain) has been shown to cause downregualtion of specific IgE synthesis, pulmonary and peripheral eosinophilia and airway hyper reactivity, and Th2→Th1 polarisation. However, therapeutic alleviation of eosinophilia by rh SP-D treatment became evident when SP-D gene deficient mice were found to be hypereosinophilic In fact, rhSP-D binds well to eosinophils derived from allergic patients and induces apoptosis without affecting eosinophils derived from healthy individuals or non-activated/non-sensitized eosinophils. Proteomic analysis of rh SP-D treated eosinophillic cell line that revealed that apoptosis induction takes place via p53 pathway. In this thesis, proteomic signatures were replicated using a leukemic cell line AML14.3D10 via qPCR analysis by identifying targets from a spectrum of genes, which were either upregulated or downregulated. It appears that in spite of induction of apoptosis by rh SP-D, different cells respond differentially at molecular levels (Chapter 3). Sensing that SP-D can induce apoptosis in altered or transformed cells; the effect of SP-D gene expression within pancreatic cancer cells was also investigated. The experiments confirmed p53 pathway dependence for suppression of cancer. Interestingly, factors responsible for metastasis for cancer are also downregulated by endogenous overexpression of SP-D, as validated by wound healing assay. We conclude that SP-D is a general immunosurveillance molecule, which is involved in the clearance of altered and transformed cells (Chapter 4). Chapter 5 shows a direct interaction between DC-SIGN and rh SP-D that inhibits DC-SIGN interaction of allergens and HIV-1, tow common ligands for SP-D and DC-SIGN. Using transfected human embryonic kidney (HEK) cells expressing surface DC-SIGN, we found that pre-treatment of these cells with rhSP-D suppressed DC-SIGN mediated transmission of HIV-1to co-cultured PBMCs. The effect of rhSP-D-DC-SIGN In conclusion, this thesis highlights a broader immune role of SP-D in homeostasis and probably assigns potential functions of extrapulmonary and/or locally synthesized SP-D within non-lung tissues and blood.
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Kaur, Anuvinder. "Innate immune surveillance in ovarian and pancreatic cancer." Thesis, Brunel University, 2017. http://bura.brunel.ac.uk/handle/2438/15847.

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Activation of innate immune surveillance mechanisms during the development of cancer is well-documented. However, knowledge of how these innate immune proteins, when added exogenously, independent of tumour microenvironment, affect tumour cells is limited. In Chapter 3, the effects of human C1q and its individual globular domains (ghA, ghB and ghC) on an ovarian cancer cell line, SKOV3, have been examined. C1q and globular head modules induced apoptosis in approximately 55% of cells, which involved upregulation of TNF-α and Fas and activation of the caspase cascade. This occurred in parallel to the downregulation of mTOR, RICTOR and RAPTOR survival pathways, which are often over-expressed in the majority of the cancers. Thus, this study provided evidence for another complement-independent role of C1q. The second part of this thesis was to investigate the effect of Human Surfactant Protein-D (SP-D), which is known to modulate secretion of a range of cytokines and chemokines by effector immune cells, such as TNF-a and TGF-β, at mucosal surfaces during infection and inflammation. Our hypothesis was that SP-D can influence these soluble factors as a part of its putative role in the immune surveillance against pancreatic cancer, where the inflammatory tumour microenvironment contributes to the epithelial-to-mesenchymal transition (EMT) invasion and metastases. In this study, a recombinant fragment of human SP-D (rfhSP-D) inhibited TGF-β expression in a range of pancreatic cancer cell lines, thereby reducing their invasive potential by downregulating Smad2/3 expression that may have interrupted signal transduction negatively, which affected the transcription of key mesenchymal genes such as Vimentin, Zeb1 and Snail. Furthermore, prolonged treatment with rfhSP-D induced apoptosis in the pancreatic cancer cell lines via activation of the caspase cascade. Thus, this study added another layer to the well-known protective role of SP-D.
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Cheung, Ann F. "Investigating immune surveillance, tolerance, and therapy in cancer." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/46809.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2009.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Vita.
Includes bibliographical references.
Maximizing the potential of cancer immunotherapy requires model systems that closely recapitulate human disease to study T cell responses to tumor antigens and to test immune therapeutic strategies. Current model systems largely relied on chemically-induced and spontaneous tumors in immunodeficient mice or on transplanted tumors. Such systems are limited because they fail to reproduce the complex interactions that exist among an emerging tumor, its microenvironment and the multiple elements of an intact immune system. We created a new system that is compatible with Cre-loxP-regulatable mouse cancer models in which the defined antigen SIY is specifically over-expressed in tumors, mimicking clinically-relevant tumor-associated antigens. To demonstrate the utility of this system, we characterized SIYreactive T cells in the context of lung adenocarcinoma, revealing multiple levels of antigenspecific T cell tolerance that serve to limit an effective anti-tumor response. Thymic deletion reduced the number of SIY-reactive T cells present in the animals. When potentially self-reactive T cells in the periphery were activated, they were efficiently eliminated. Inhibition of apoptosis resulted in more persistent self-reactive T cells, but these cells became anergic to antigen stimulation. Finally, in the presence of tumors over- expressing SIY, SIY-specific T cells required a higher level of costimulation to achieve functional activation.
(cont.) Adoptive cell transfer (ACT) therapy for cancer has demonstrated tremendous efficacy in clinical trials, particularly for the treatment of metastatic melanoma. There is great potential in broadening the application of ACT to treat other cancer types, but the threat of severe autoimmunity may limit its use. Studies in other model systems have demonstrated successful induction of anti-tumor immunity against self-antigens without detrimental autoimmunity. This is possibly due to the preferential recognition of tumor over normal somatic tissue by activated T cells. In our system, SIY provides a means to achieve this bias because of its over-expression in tumors. Thus, we applied adoptive T cell transfer therapy combined with lymphodepleting preconditioning to treat autochthonous lung tumors over-expressing SIY self-antigen. With this treatment, we overcame peripheral tolerance, successfully inducing large number of functional anti-tumor T cells. These T cells are able to influence lung tumors over-expressing self-antigen. Importantly, despite large numbers of potentially self-reactive T cells, we did not observed overt autoimmunity. Immune tolerance thwarts efforts to utilize immune therapy against cancer. We have discerned many mechanisms by which tolerance to cancer in potential achieved. Both Foxp3+ T regulatory cell and myeloid-derived suppressor cell populations are expanded in the presence of cancer in our mouse models.
(cont.) In addition, we identified LAG-3 as a potential factor that serves to limit anti-tumor T cell activity in the context of adoptive cell transfer therapy. Our new system represents a valuable tool in which to explore the mechanisms that contribute to T cell tolerance to cancer and to evaluate therapies aimed at overcoming this tolerance. In addition, our model provides a platform, on which more advanced mouse models of human cancer can be generated for cancer immunology.
by Ann F. Cheung.
Ph.D.
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Loughhead, Scott McNabb. "Immune Surveillance by Effector and Memory CD8+ T Cells." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:26718721.

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During priming, CD8+ T cells integrate a plethora of signals that affect their differentiation into subsets of CD8+ T cells with distinct migratory properties and functions. Given that CD8+ T cells exert their protective function via cell-cell contacts, the migratory patterns and spatial distribution of CD8+ T cell subsets induced by primary challenge are of critical importance to the host. Dendritic cells (DCs), as the primary initiators of these responses, play a pivotal role in shaping the size and differentiation status of CD8+ T cells that emerge. However, inadequate markers for CD8+ T cell subsets have hindered study of their lineage relationships, as well as their migratory behaviors. Here, we use a novel marker for identification of CD8+ T cell subsets to interrogate whether subsets of DCs skew CD8+ T cell fate decisions, the differentiation pattern of CD8+ T cell subsets, and the migratory behavior of these CD8+ T cell subsets. Within secondary lymphoid organs (SLOs), CD8+ T cells encounter subsets of DCs that may differentially impact subsequent T cell fate decisions. While distinct DC subsets were found to influence CD8+ T cell priming and subsequent differentiation in vitro, these differences were masked when priming occurred in vivo. This prompted us to delve deeper into how CD8+ T cell subsets are defined in vivo. Classically, memory CD8+ T cells are divided into two subsets: central memory T cells (TCM) and effector memory T cells (TEM). Based on the variable expression of the chemokine receptor, CX3CR1, we define TCM as CX3CR1- and TEM as CX3CR1high. Additionally, a previously undefined subset of T cells was identified that express intermediate levels of CX3CR1. Flow cytometric analysis of the subsets migrating through murine peripheral tissues in the memory phase established CX3CR1int cells as the dominant subset, thus these cells have been termed peripheral memory T cells (TPM). Lineage tracing of these three subsets established a uni-directional relationship where increasing levels of CX3CR1 marked further terminal differentiation: TCM (CX3CR1-) to TPM (CX3CR1int) to TEM (CX3CR1hi). The finding that TPM, and not TEM, migrated through peripheral tissues was intriguing because it contradicted previous studies suggesting that TEM had this migratory pattern. To resolve this contradiction, we visualized the migration of TEM precursors, CX3CR1hi effector T cells (TEff), by intravital multi-photon microscopy (IV-MPM) in real-time. Surprisingly, CX3CR1hi TEff adhered to and patrolled along the dermal endothelium of mice. Specifically, migration was enriched along arteriolar endothelium and tended to be against blood flow. Patrolling occurred for both CX3CR1hi TEff and TEM and was limited to CX3CR1hi CD8+ T cells and CX3CR1hi monocytes, but was not dependent on functional CX3CR1. Moreover, addition of cognate antigen (Ag) resulted in rapid stopping of Ag-specific T cells, suggesting that patrolling T cells scan arteriolar endothelium for cognate Ag. Together, these results challenge the paradigm that TEM function by migration through peripheral tissues and establish a new migratory behavior by TEM and their effector precursors that promotes intravascular scanning of arteriolar endothelium.
Medical Sciences
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Sowinski, Stefanie. "Transmission and immune surveillance of human T cell-tropic retroviridae." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501764.

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Textor, Johannes [Verfasser]. "Search and learning in the immune system : models of immune surveillance and negative selection / Johannes Textor." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2012. http://d-nb.info/1024336921/34.

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Blaimer, Stephanie [Verfasser], and Edward K. [Akademischer Betreuer] Geissler. "Impact of innate and adaptive immune cells in tumor immune surveillance / Stephanie Blaimer ; Betreuer: Edward K. Geissler." Regensburg : Universitätsbibliothek Regensburg, 2020. http://d-nb.info/1210729202/34.

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Strickland, Ian. "The role of immune surveillance in inflammatory reactions in human skin." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307670.

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Books on the topic "Surveillance immune"

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Sonnenfeld, Gerald. Cytokines and immune surveillance in humans: Fifth semi-annual progress report. [Washington, DC: National Aeronautics and Space Administration, 1993.

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Smith, Richard T. Immune Surveillance. Elsevier Science & Technology Books, 2012.

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Cytokines and immune surveillance in humans. [Washington, DC: National Aeronautics and Space Administration, 1994.

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Kishore, Uday, Roberta Bulla, and Taruna Madan, eds. Odyssey of Surfactant Proteins SP-A and SP-D: Innate Immune Surveillance Molecules. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-680-8.

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Epidemiological surveillance of current infections: new threats and challenges. Remedium Privolzhye, 2021. http://dx.doi.org/10.21145/978-5-6046124-2-2_2021.

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The collection contains the scientific works of the All-Russian Scientific and Practical conference «Epidemiological surveillance of current infections: new threats and challenges», held by the FBIS «Academician I.N. Blokhina Nizhny Novgorod Scientific Research Institute of Epidemiology and Microbiology» of Rospotrebnadzor in honor of the 100th anniversary of the outstanding scientist I. N. Blokhina, who headed the Institute for 44 years. Leading scientists and specialists from 57 scientific and practical institutions of Rospotrebnadzor, healthcare, education and other organizations from 32 regions of Russia and foreign countries took part in the compilation of the materials. The materials of the collection present the results of scientific research on the epidemiology of current infections, including the use of GIS technologies, methods of molecular epidemiology and bioinformatics, achievements in the field of diagnostics, molecular genetic and molecular biological studies of pathogens of bacterial and viral nature, in the study of human immune defense mechanisms, means of ensuring biological safety, general and population ecology of microorganisms of various biosystems, a number of aspects of biotechnology of immunobiological drugs, etc A separate section of the collection is devoted to new threats to the safety of the population, among them the most relevant is the pandemic of a new coronavirus infection. The collection contains materials on the results of studies on the pathogenesis, epidemiology, clinic and diagnosis of COVID-19. The conference materials will be useful for both scientific and practical employees of Rospotrebnadzor institutions, other ministries and departments involved in the work of the system of anti-epidemic protection of the population, as well as epidemiologists, microbiologists, virologists, biotechnologists, etc. working in various fields of science, education and practical health care. Scientific articles are published in the author’s edition.
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Cate, Fred H., and James X. Dempsey, eds. Bulk Collection. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190685515.001.0001.

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In June 2013, Edward Snowden revealed a secret US government program that collected records on every phone call made in the country. Further disclosures followed, detailing mass surveillance by the UK as well. Journalists and policymakers soon began discussing large-scale programs in other countries. Over two years before the Snowden leaks began, Cate and Dempsey had started researching systematic collection. Leading an initiative sponsored by The Privacy Projects, they commissioned a series of country reports, asking national experts to uncover what they could about government demands that telecommunications providers and other private-sector companies disclose information about their customers in bulk. Their initial research found disturbing indications of systematic access in countries around the world. These programs, often undertaken in the name of national security, were cloaked in secrecy and largely immune from oversight, posing serious threats to personal privacy. After the Snowden leaks, the project morphed into something more ambitious: an effort to explore what should be the rules for government access to data and how companies should respond to those demands within the framework of corporate responsibility. This volume concludes the nearly six-year project. It assembles 12 country reports, updated to reflect recent developments. One chapter presents both descriptive and normative frameworks for analyzing national surveillance laws. Others examine international law, human rights law, and oversight mechanisms. Still others explore the concept of accountability and the role of encryption in shaping the surveillance debate. In their conclusion, Cate and Dempsey offer recommendations for both government and industry.
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Dalbeth, Nicola. Pathophysiology of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0039.

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The clinical features of gout occur in response to monosodium urate (MSU) crystals. Gout should be considered a chronic disease of MSU crystal deposition. A number of pathophysiological checkpoints are required for development of gout. First, elevated urate concentrations are required: urate overproduction and underexcretion contribute to total urate balance. Overproduction occurs due to alterations in the purine synthesis and degradation pathways. Renal underexcretion is an important cause of elevated serum urate concentrations (hyperuricaemia), and occurs through alterations in the urate transporters within the renal tubule (collectively known as the urate transportasome). Gut underexcretion (extrarenal urate underexcretion) also contributes to development of hyperuricaemia. The next checkpoint is MSU crystal formation. In some individuals with evidence of MSU crystal deposition, symptomatic gout develops. The acute inflammatory response to MSU crystals represents a self-limiting sterile acute auto-inflammatory response which is mediated by the innate immune system activation. Interleukin 1 beta is the key cytokine that contributes to the acute inflammatory response to MSU crystals. In some patients, advanced gout may occur with structural joint damage. Joint damage in gout is mediated both by direct effects of MSU crystals on joint tissue and by indirect effects of joint inflammation. In addition to their central role in pathogenesis of gout, MSU crystals have a physiological role, particularly as an adjuvant or ‘danger signal’ in immune surveillance.
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Sherman, Mark E., Melissa A. Troester, Katherine A. Hoadley, and William F. Anderson. Morphological and Molecular Classification of Human Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0003.

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Accurate and reproducible classification of tumors is essential for clinical management, cancer surveillance, and studies of pathogenesis and etiology. Tumor classification has historically been based on the primary anatomic site or organ in which the tumor occurs and on its morphologic and histologic phenotype. While pathologic criteria are useful in predicting the average behavior of a group of tumors, histopathology alone cannot accurately predict the prognosis and treatment response of individual cancers. Traditional measures such as tumor stage and grade do not take into account molecular events that influence tumor aggressiveness or changes in the tumor composition during treatment. This chapter provides a primer on approaches that use pathology and molecular biology to classify and subclassify cancers. It describes the features of carcinomas, sarcomas, and malignant neoplasms of the immune system and blood, as well as various high-throughput genomic platforms that characterize the molecular profile of tumors.
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Stewart, Alex G., Sam Ghebrehewet, and Peter MacPherson. New and emerging infectious diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198745471.003.0026.

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This chapter describes the increasing global problem of new and emerging infections, many zoonotic, ranging from the recently described Middle East respiratory syndrome (MERS) to bacteria now resistant to all locally available antimicrobial agents. The environmental, human, technological, and microbial factors contributing to disease emergence are assessed. Changes in environment and land use result in the spread of vector-borne diseases into new areas, and global travel and trade may introduce pathogens to non-immune populations. The breakdown of health services following political change or during conflict can result in the resurgence of previously controlled communicable diseases. The importance of collaboration between human and veterinary health services is emphasized, and the UK ‘DATER’ strategy (Detection, Assessment, Treatment, Escalation, Recovery) for dealing with pandemic influenza is applied to new and emerging infections. Finally, the role of internet-based, syndromic surveillance to create early awareness of new infections is considered.
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Book chapters on the topic "Surveillance immune"

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Mitchison, N. A. "Immune Surveillance." In Investigation and Exploitation of Antibody Combining Sites, 335. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5006-4_40.

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Koga, Tetsuya. "Immune Surveillance against Dermatophyte Infection." In Fungal Immunology, 443–52. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-25445-5_22.

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Jung, M. Katherine. "Immune Surveillance and Tumor Evasion." In Alcohol and Cancer, 193–210. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0040-0_10.

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Mastrangelo, Domenico. "Immune Surveillance and Cancer Pathogenesis." In Orbital Tumors, 9–20. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1510-1_2.

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Roy, Moumita. "Alternative Splicing and Immune Surveillance." In Alternative Splicing and Cancer, 125–44. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003260394-8.

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Huso, David L., and Opendra Narayan. "Escape of Lentiviruses from Immune Surveillance." In Virus Variability, Epidemiology and Control, 61–73. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9271-3_5.

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Uenotsuchi, Takeshi, Tetsuo Matsuda, Masutaka Furue, and Tetsuya Koga. "Immune Surveillance against Sporothrix schenckii Infection." In Fungal Immunology, 453–58. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-25445-5_23.

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Van den Eynde, B., B. Lethé, A. Van Pel, and T. Boon. "Tumor Rejection Antigens and Immune Surveillance." In Modern Trends in Human Leukemia IX, 279–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76829-3_42.

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Chen, Peter W., and Bruce R. Ksander. "Influence of Immune Surveillance and Immune Privilege on Formation of Intraocular Tumors." In Immune Response and the Eye, 276–89. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000099278.

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Paape, Max J., Kimberly Shafer-Weaver, Anthony V. Capuco, Kaat Van Oostveldt, and Christian Burvenich. "Immune Surveillance of Mammary Tissue by Phagocytic Cells." In Biology of the Mammary Gland, 259–77. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46832-8_31.

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Conference papers on the topic "Surveillance immune"

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Dudimah, Duafalia F., Roman V. Uzhachenko, Samuel T. Pellom, Asel K. Biktasova, Mikhail M. Dikov, David P. Carbone, and Anil Shanker. "Abstract 3983: Resuscitating immune surveillance in cancer." 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.am2013-3983.

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Agudo, Judith, Miriam Merad, and Brian D. Brown. "Abstract A168: Quiescent stem cells evade immune surveillance." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a168.

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Bandyopadhyay, G., H. L. Huyck, S. Bhattacharya, R. Misra, J. Lillis, J. Myers, S. Romas, et al. "Respiratory Epithelial Cell Regulation of Pulmonary Immune Surveillance." 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.a2130.

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Kuttke, Mario, Emine Sahin, Julia Pisoni, Sophie Percig, Andrea Vogel, Daniel Kraemmer, Leslie Hanzl, et al. "Abstract 527: Myeloid PTEN deficiency impairs tumor immune surveillance via immune checkpoint inhibition." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-527.

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Razia, D., H. Abdelrazek, H. Mohamed, and A. Arjuna. "De Novo Prostate Adenocarcinoma in a Lung Transplant Recipient: Immune-surveillance or Immune-suppression?" In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5219.

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Dudimah, Duafalia F., Samuel T. Pellom, Roman V. Uzhachenko, David P. Carbone, Mikhail M. Dikov, and Anil Shanker. "Abstract 3642: Cancer therapy by resuscitating Notch immune surveillance." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3642.

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Zal, M. Anna, Todd Bartkowiak, Grzegorz Chodaczek, Veena Papanna, Meenakshi Shanmugasundaram, and Tomasz Zal. "Abstract 4290: Visualizing immune surveillance in lung metastasis progression." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4290.

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Johnstone, Ricky W. "Abstract IA25: Epigenetic regulation of cancer immune surveillance processes." In Abstracts: Second AACR Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; May 6-9, 2017; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.hemmal17-ia25.

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Vonderheide, Robert H. "Abstract SY09-01: Inflammatory networks and cancer immune surveillance." 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-sy09-01.

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Bardelli, Alberto. "Abstract IA18: Inactivation of DNA repair to improve immune surveillance." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-ia18.

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Reports on the topic "Surveillance immune"

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Luo, Yunping, and Ralph A. Reisfeld. Priming the Tumor Immune Microenvironment Improves Immune Surveillance of Cancer Stem Cells and Prevents Cancer Recurrence. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada574527.

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Reisfeld, Ralph R., Debbie Liao, and Yunping Luo. Priming the Tumor Immune Microenvironment Improves Immune Surveillance of Cancer Stem Cells and Prevents Cancer Recurrence. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada553886.

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Bovbjerg, Dana H. Immune Surveillance, Cytokines and Breast Cancer Risk: Genetic and Psychological Influences in African American Women. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada418645.

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Bovbjerg, Dana H. Inherited Susceptibility to Breast Cancer in Healthy Women: Mutation in Breast Cancer Genes, Immune Surveillance, and Psychological Distress. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada403466.

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Bovbjerg, Dana H. Inherited Susceptibility to Breast Cancer in Healthy Women: Mutation in Breast Cancer Genes, Immune Surveillance, and Psychological Distress. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada427835.

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Bovbjerg, Dana H. Inherited Susceptibility to Breast Cancer in Healthy Women: Mutation in Breast Cancer Genes, Immune Surveillance, and Psychological Distress. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada431795.

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Bovbjerg, Dana H. Inherited Susceptibility to Breast Cancer in Healthy Women: Mutation in Breast Cancer Genes, Immune Surveillance, and Psychological Distress. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada410581.

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Gupte, Jaideep, Sarath MG Babu, Debjani Ghosh, Eric Kasper, and Priyanka Mehra. Smart Cities and COVID-19: Implications for Data Ecosystems from Lessons Learned in India. Institute of Development Studies (IDS), March 2021. http://dx.doi.org/10.19088/sshap.2021.034.

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This brief distils best data practice recommendations through consideration of key issues involved in the use of technology for surveillance, fact-checking and coordinated control during crisis or emergency response in resource constrained urban contexts. We draw lessons from how data enabled technologies were used in urban COVID-19 response, as well as how standard implementation procedures were affected by the pandemic. Disease control is a long-standing consideration in building smart city architecture, while humanitarian actions are increasingly digitised. However, there are competing city visions being employed in COVID-19 response. This is symptomatic of a broader range of tech-based responses in other humanitarian contexts. These visions range from aspirations for technology driven, centralised and surveillance oriented urban regimes, to ‘frugal innovations’ by firms, consumers and city governments. Data ecosystems are not immune from gendered- and socio-political discrimination, and technology-based interventions can worsen existing inequalities, particularly in emergencies. Technology driven public health (PH) interventions thus raise concerns about 1) what types of technologies are appropriate, 2) whether they produce inclusive outcomes for economically and socially disadvantaged urban residents and 3) the balance between surveillance and control on one hand, and privacy and citizen autonomy on the other.
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Gupte, Jaideep, Sarath MG Babu, Debjani Ghosh, Eric Kasper, Priyanka Mehra, and Asif Raza. Smart Cities and COVID-19: Implications for Data Ecosystems from Lessons Learned in India. Institute of Development Studies, March 2022. http://dx.doi.org/10.19088/sshap.2022.004.

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This brief distils best data practice recommendations through consideration of key issues involved in the use of technology for surveillance, fact-checking and coordinated control during crisis or emergency response in resource constrained urban contexts. We draw lessons from how data enabled technologies were used in urban COVID-19 response, as well as how standard implementation procedures were affected by the pandemic. Disease control is a long-standing consideration in building smart city architecture, while humanitarian actions are increasingly digitised. However, there are competing city visions being employed in COVID-19 response. This is symptomatic of a broader range of tech-based responses in other humanitarian contexts. These visions range from aspirations for technology driven, centralised and surveillance oriented urban regimes, to ‘frugal innovations’ by firms, consumers and city governments. Data ecosystems are not immune from gendered- and socio-political discrimination, and technology-based interventions can worsen existing inequalities, particularly in emergencies. Technology driven public health (PH) interventions thus raise concerns about 1) what types of technologies are appropriate, 2) whether they produce inclusive outcomes for economically and socially disadvantaged urban residents and 3) the balance between surveillance and control on one hand, and privacy and citizen autonomy on the other.
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Gupte, Jaideep, Sarath MG Babu, Debjani Ghosh, Eric Kasper, Priyanka Mehra, and Asif Raza. Smart Cities and COVID-19: Implications for Data Ecosystems from Lessons Learned in India. SSHAP, March 2021. http://dx.doi.org/10.19088/sshap.2021.012.

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Abstract:
This brief distils best data practice recommendations through consideration of key issues involved in the use of technology for surveillance, fact-checking and coordinated control during crisis or emergency response in resource constrained urban contexts. We draw lessons from how data enabled technologies were used in urban COVID-19 response, as well as how standard implementation procedures were affected by the pandemic. Disease control is a long-standing consideration in building smart city architecture, while humanitarian actions are increasingly digitised. However, there are competing city visions being employed in COVID-19 response. This is symptomatic of a broader range of tech-based responses in other humanitarian contexts. These visions range from aspirations for technology driven, centralised and surveillance oriented urban regimes, to ‘frugal innovations’ by firms, consumers and city governments. Data ecosystems are not immune from gendered- and socio-political discrimination, and technology-based interventions can worsen existing inequalities, particularly in emergencies. Technology driven public health (PH) interventions thus raise concerns about 1) what types of technologies are appropriate, 2) whether they produce inclusive outcomes for economically and socially disadvantaged urban residents and 3) the balance between surveillance and control on one hand, and privacy and citizen autonomy on the other.
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