Relevant bibliographies by topics / System immunology

Academic literature on the topic 'System immunology'

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Published: 10 March 2023

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Journal articles on the topic "System immunology"

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Wickelgren, I. "IMMUNOLOGY: Policing the Immune System." Science 306, no. 5696 (October 22, 2004): 596–99. http://dx.doi.org/10.1126/science.306.5696.596.

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Keane, Robert W., and William F. Hickey. "Immunology of the Nervous System." Journal of Neuropathology and Experimental Neurology 57, no. 1 (January 1998): 95. http://dx.doi.org/10.1097/00005072-199801000-00011.

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Villani, Alexandra-Chloé, Siranush Sarkizova, and Nir Hacohen. "Systems Immunology: Learning the Rules of the Immune System." Annual Review of Immunology 36, no. 1 (April 26, 2018): 813–42. http://dx.doi.org/10.1146/annurev-immunol-042617-053035.

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Poon, Maya M. L., and Donna L. Farber. "The Whole Body as the System in Systems Immunology." iScience 23, no. 9 (September 2020): 101509. http://dx.doi.org/10.1016/j.isci.2020.101509.

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Carty, Shannon A. "Immunology 101: fundamental immunology for the practicing hematologist." Hematology 2021, no. 1 (December 10, 2021): 281–86. http://dx.doi.org/10.1182/hematology.2021000260.

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Abstract From an evolutionary perspective, the immune system developed primarily to protect the host from pathogens. In the continuous balance between killing pathogens and protecting host tissues, selective pressures have shaped the discriminatory functions of the immune system. In addition to protection against microbial pathogens, the immune system also plays a critical role in antitumor immunity. Immune dysfunction, either under- or overactivity, is found in a wide range of hematologic disorders. Here we review the fundamental features of the immune system and the key concepts critical to understanding the impact of immune dysfunction on hematologic disorders.
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MALIM, MUHAMMAD ROZI, and FARIDAH ABDUL HALIM. "IMMUNOLOGY AND ARTIFICIAL IMMUNE SYSTEMS." International Journal on Artificial Intelligence Tools 21, no. 06 (December 2012): 1250031. http://dx.doi.org/10.1142/s0218213012500315.

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Artificial immune system is inspired by the natural immune system for solving computational problems. The immunological principles that are primarily used in artificial immune systems are the clonal selection principle, the immune network theory, and the negative selection mechanism. These principles have been applied in anomaly detection, pattern recognition, computer and network security, dynamic environments and learning, robotics, data analysis, optimization, scheduling, and timetabling. This paper describes how these three immunological principles were adapted by previous researchers in their artificial immune system models and algorithms. Finally, the applications of various artificial immune systems to various domains are summarized as a time-line.
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KOBAYASHI, JUNZO. "Immunology on the digestive system.3.Inflammatory enteric diseases and immunology." Nihon Naika Gakkai Zasshi 82, no. 9 (1993): 1394–98. http://dx.doi.org/10.2169/naika.82.1394.

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Pineda, Silvia, Daniel G. Bunis, Idit Kosti, and Marina Sirota. "Data Integration for Immunology." Annual Review of Biomedical Data Science 3, no. 1 (July 20, 2020): 113–36. http://dx.doi.org/10.1146/annurev-biodatasci-012420-122454.

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Over the last several years, next-generation sequencing and its recent push toward single-cell resolution have transformed the landscape of immunology research by revealing novel complexities about all components of the immune system. With the vast amounts of diverse data currently being generated, and with the methods of analyzing and combining diverse data improving as well, integrative systems approaches are becoming more powerful. Previous integrative approaches have combined multiple data types and revealed ways that the immune system, both as a whole and as individual parts, is affected by genetics, the microbiome, and other factors. In this review, we explore the data types that are available for studying immunology with an integrative systems approach, as well as the current strategies and challenges for conducting such analyses.
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THOMAS, A. J. "Immunology of The Male Reproductive System." Cleveland Clinic Journal of Medicine 55, no. 6 (November 1, 1988): 567. http://dx.doi.org/10.3949/ccjm.55.6.567.

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Tambur, A. R., and B. Roitberg. "Immunology of the central nervous system." Neurological Research 27, no. 7 (October 2005): 675–78. http://dx.doi.org/10.1179/016164105x49544.

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Dissertations / Theses on the topic "System immunology"

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Hanke, Mark L. "Sympathetic Nervous System Mediated Alterations in the Immunological and Behavioral Effects of Social Defeat." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1283527905.

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Bell, Michael David. "Factors regulating inflammation in the central nervous system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308694.

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Babiker, Adil Abdelgadir. "Prostasome Modulation of Blood Cascade System and Phosphoprotein Reactions with Focus on Prostate Cancer." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5779.

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Hassan-Zahraee, Mina. "Anergy and the human skin immune system." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42051.

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An initial study comparing cytokine gene expression in the skin of control vs. anergic patients lacking delayed type hypersensitivity reactivity revealed no difference; but disclosed an apparent absence of detectable CD3+ T cells in the skin of anergic individuals. To assess its significance for anergy, an investigation of the role of skin T cells in DTH-reactive healthy individuals was undertaken. To do so, the phenotypic and functional characteristics of T cells isolated from skin and blood were compared. Analysis by flow cytometry has shown that 74% of skin T cells expressed cell surface HLADR, 66% were positive for the IL-2 receptor CD25, and less than 43% have displayed the VLA integrin $ alpha$4 chain as compared to 28%, 7%, 79% for peripheral blood mononuclear cells respectively. The expression of a cutaneous lymphocyte antigen (CLA) was 61% in the former and 14% in the latter. Functionally, skin T cells failed to proliferate in response to all ligands including IL-2, anti-CD3, lectins and phorbol esters with ionomycin, as well as showed a reduced Ca++ flux to phytohemagglutinin. Skin tissue co-cultured with autochtonous PBL could inhibit its proliferative reaction. Despite their ability to proliferate, lymphocytes from skin were shown to be able to produce IFN$ gamma$ in response to PHA+IL-12 as well as anti-CD3+IL-2. Inhibition by anti-cytokine mAbs revealed that in both instances IL-12 was obligatory for this production. In an additional study it was established that a hitherto uncharacterized subset of T cells in blood which could secrete IFN$ gamma$ consisted of CLA+ cells. This observation established a functional link between these CLA+ skin-seeking T cells and the CLA+ T cells in skin.
A major difference between IFN$ gamma$-producing cells from blood and skin was found to be the tempo of synthesis: whereas, PBMC was first detected to contain IFN$ gamma$ 42 hours following activation, lasting for days, skin cells were positive after 2.5 hrs of activation, (or 16x faster) for a duration of only 90 minutes. These kinetics were confirmed using intact skin in culture. Experiments designed to reveal the mechanism of this fast action have shown that mRNA for IFN$ gamma$ is present in unstimulated isolated skin T cells as well as in intact skin, but not in PBMC, and its presence may be attributed to ongoing constitutive transcription. Activation of skin T cells, which has been shown to elicit prompt translation in IFN$ gamma$ synthesis has also been shown, at the same time, to terminate IFN$ gamma$ gene transcription in an apparently selective manner. Accordingly, it can be seen that the amount of IFN$ gamma$ synthesized in skin and the duration of its synthesis is preprogrammed. This mode of regulation may be unique to the skin, and unique for IFN$ gamma.$
The results presented are interpreted to indicate that r cells present in human skin may play an essential role in the DTH response, and provide evidence for "peripheral sensitization", or lymphocyte activation outside organized lymphoid tissue. Because of its speed, it may represent the antigen-specific component of a first line cutaneous host defence system. The absence of such T cells in the skin of anergic patients may indeed be responsible for a lack of DTH reactivity, and its clinical consequences.
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Brown, Heidi Catherine. "Macrophages and the nervous system." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320118.

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Sefik, Esen. "Individual Microbes Shape Various Parts of the Immune System." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845459.

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The gastrointestinal tract, home to a vast number of bacteria, requires finely-tuned regulatory and effector immune mechanisms to maintain homeostasis and tolerance. In a large-scale screen, we studied the impacts of single microbes on major immune populations, whole intestinal tissue homeostasis and metabolism. Bacteria interacted with the host at multiple levels including cytokine responses, accumulation of various T cells, alterations in composition of mononuclear phagocytes and induction of epithelial cell genes as measured by transcriptome analysis of whole intestinal tissue. Interestingly, taxonomically unrelated bacteria elicited similar immune phenotypes and metabolic effects. A more focused analysis of the induction of regulatory mechanisms revealed a microbiota-dependent, context-specific transcriptional control of Foxp3+ regulatory T cells and of IL17 producing T cells. These facets were both regulated by Rorγ, a transcription factor known for its antagonistic effects on Foxp3. Paradoxically, Rorγ expression induced by bacteria in colonic Foxp3+ regulatory T cells was necessary for function of these cells especially in the context of IL17 and IFNγ-mediated colitis. Overall, this large-scale screen provides a comprehensive study of how individual bacterial species shape many aspects of the host immunity and metabolism, and exemplifies a microbiota-dependent, context-specific mechanism that potentiates function in Foxp3+ regulatory T cells.
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Babcock, Alicia A. "The innate response to injury in the central nervous system /." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111817.

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Innate responses in the central nervous system (CNS) provide first-line defense against infection and injury. Microglia and astrocytes may direct leukocyte infiltration to the injured CNS. The signaling mechanisms that orchestrate this response are ill-defined. Innate roles for microglia and astrocytes are supported by reports demonstrating glial expression of Toll-like receptors (TLRs). TLRs recognize conserved pathogen-associated motifs and generate innate immune responses, usually by signaling through the adaptor protein, MyD88. TLRs may also generate innate responses to tissue damage. The data in this thesis implicate TLR2/MyD88 as key mediators of innate response to brain injury in mice. Transection of axons in the entorhinal cortex causes tissue damage analogous to a stab injury at the lesion site, and axonal degeneration distal from the wound, in the denervated, lesion-reactive hippocampus. A significant increase in leukocyte proportions was detected by 3h in the stab-injured entorhinal cortex, but not until 12h in the denervated hippocampus. This identified a window of CNS-directed innate response in the denervated hippocampus, without influence of infiltrating cells. Expression of numerous cytokines and chemokines was induced during this time. Microglia and astrocytes were identified as major sources of the chemokine CCL2. Macrophage infiltration to the stab-injured entorhinal cortex and the denervated hippocampus was dependent on MyD88-dependent CCL2/CCR2 signaling, but not TLR2-signalled response. T cell entry to the denervated hippocampus was regulated by TLR2 signaling and required MyD88-mediated response, whereas T cell recruitment to the stabinjured entorhinal cortex was only partially dependent on MyD88 signaling and did not require TLR2-mediated response. TLR2 signaling also regulated expansion of the hippocampal microglial population 5 days after lesion. Microglia were supplemented by circulating bone marrow-derived precursors, but this occurred predominantly at later times post-injury. No parameter measured was dependent on TLR4. These data identify novel signaling pathways that link glial responses to brain injury with subsequent neuroinflammation.
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Drennan, Michael B. "Mycobacterium tuberculosis and trypanosoma brucei as models for the TLR-dependent activation of the innate immune system." Doctoral thesis, University of Cape Town, 2005. http://hdl.handle.net/11427/3111.

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Kristjánsdóttir, Helga. "The PD-1 pathway and the complement system in systemic lupus erythematosus." Doctoral thesis, Uppsala universitet, Medicinsk genetik, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-107198.

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Autoimmune diseases occur in up to 3-5% of the general population and represent a diverse collection of diseases with regards to clinical manifestations. The unifying factor of autoimmune diseases is tissue and organ damage as a result of an immune response mounted against self-antigens. Systemic lupus erythematosus (SLE) is considered a prototype of human systemic autoimmune diseases. The etiology of SLE is as yet largely unknown, but both epidemiological and genetic data suggest an interplay between numerous and varying genetic and environmental factors. There is compelling evidence for a strong genetic component in SLE. The disease has a high λsibs value and familial clustering is apparent. Multiple susceptibility loci have been identified, some of which are syntenic between humans and mice and some of which overlap with other autoimmune diseases.   This thesis is based on analysis of Icelandic multicase SLE families and Swedish SLE patients. Paper I is a study of the association of C4A protein deficiency (C4AQ0) with SLE in the multicase families and shows a significantly increased frequency of C4AQ0 in the families. The genetic basis for C4AQ0 varies and C4AQ0 is found on different MHC haplotypes, pointing to C4AQ0 as an independent risk factor for SLE. Paper II describes the association of low MBL serum levels with SLE in the families and identifies low MBL as risk factor for SLE in families that carry the defect. Low MBL was furthermore found to mediate an additive risk when found in combination with C4AQ0. In paper III cellular expression the PD-1 co-inhibitory receptor on T cells was studied. A polymorphism in the PDCD1 gene, PD-1.3A was previously associated with SLE in the multicase families. The polymorphism is thought to disrupt expression of the gene and may lead to decreased expression of the PD-1 receptor. The study demonstrates lower PD-1 expression in SLE patients and relatives in correlation to the PD-1.3A genotype. Paper IV is a compiled analysis of the SLE families, including PD-1.3A, C4AQ0, low MBL, autoimmune diseases and autoantibody profiles. The study demonstrates clustering of different autoimmune diseases and autoantibodies in families that are heterogenic with regards to the genetic susceptibility factors, PD-1.3A, C4AQ0 and low MBL.
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Doody, Karen. "T cell protein tyrosine phosphatase in immune system development and disease." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104657.

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The ontogeny of the immune system is orchestrated by a highly organized cell signaling network that ensures the development of multiple hematopoietic lineages and allows them to transduce information from their environment in order to mount appropriate responses to prevent disease. The phosphotyrosine signaling network has developed in higher organisms and is undeniably central to the immune system; alterations in components of this network, such as protein tyrosine phosphatases (PTP), can lead to immunodeficiency, autoimmune disease, and hematopoietic malignancy. The T cell protein tyrosine phosphatase (TC-PTP; gene name PTPN2) is highly expressed in hematopoietic tissues, and is involved in the development of several hematopoietic lineages. This thesis addresses the role of TC-PTP in immune system development and disease through the study of a TC-PTP knockout mouse model system. While TC-PTP contains a highly conserved catalytic PTP motif and shares high homology with its family member PTP1B, I have found that these two PTPs are complementary yet non-redundant during embryogenesis as well as myelopoiesis and T cell lymphopoiesis, and thus TC-PTP has a unique function in these processes. Next, I demonstrate that TC-PTP deficiency in mice leads to severe subchondral bone resorption and synovitis. These manifestations resemble early arthritis, and support recent genome wide association studies that identify SNPs in the PTPN2 locus. Finally, I identify the cell autonomous defect involved in the block of B cell development in TC-PTP-/- mice. B cells lacking TC-PTP have increased basal levels of apoptosis as well as increased sensitivity to DNA damage; in addition, these cells have defective V(D)J recombination, suggesting that the apoptosis in TC-PTP-/- progenitor B cells may arise from sensitivity to V(D)J recombination at this stage of development. Such observations elicit interest to study TC-PTP in leukemia development, therefore I also describe the analysis of TC-PTP expression levels in human B cell acute lymphoblastic leukemia in order to address these questions. The research presented herein provides valuable information on the role of TC-PTP in immune system development as well as its role in human immune disease.
L'ontogénie du système immunitaire est assurée par un réseau de signalisation complexe qui permet le développement des lignées cellulaire hématopoïétiques, la traduction d'information provenant de l'environnement de la cellule ainsi que la production d'une réponse prévenant tout apparition d'anormalité. Le réseau de phosphorylation protéique des résidues tyrosines, est présent chez les organismes développés et joue un rôle primordiale au niveau du système immunitaire. Les altérations affectant les membres de ce réseau, incluant les protéines tyrosine phosphatases (PTPs), peuvent mener à une déficience immunitaire, des maladies auto-immunes ainsi que des malignités hématopoïétiques. La PTP des cellules T (TC-PTP, nom de gène PTPN2) est une tyrosine phosphatase ubiquitairement exprimée, mais prédominante dans les tissues hématopoïétiques chez lesquels elle assure une fonction primordiale, particulièrement durant leur croissance. Cette thèse adresse le rôle particulier de TC-PTP dans le développement du système immunitaire et ses maladies en utilisant un modèle de souris knock-out (KO) de cette phosphatase. TC-PTP est reconnue pour son homologie avec la protéine tyrosine phosphatase 1B (PTP1B) et toutes deux possèdent un domaine catalytique similaire qui est conservé chez les PTPs. Malgré ces homologies, j'ai pu démontrer que ces deux PTPs ont des fonctions complémentaires et non redondantes au niveau du développement embryonnaire, de la myélopoïèse et de la lymphopoïèse des cellules T. Ainsi, TC-PTP possède un rôle unique dans les processus précédemment énumérés. Par la suite, j'ai démontré qu'une déficience de TC-PTP chez la souris mène à une résorption osseuse sous-chondrale ainsi qu'une synovite, deux phénotypes ressemblant aux symptômes observés durant les premiers stages de développement de l'arthrite. Ces découvertes supportent de récentes études génomiques associant plusieurs polymorphismes situés dans le locus de PTPN2 à différentes maladies auto-immunes. Finalement, j'ai pu identifier chez la souris TC-PTP-/- le défaut spécifique à la cellule en-soi et non son environnement qui est responsable du blocage observé durant le développement des cellules B. Ces dernières n'exprimant pas TC-PTP ont un niveau basal plus élevé de mort cellulaire ainsi qu'une grande sensibilité au dommage à l'ADN. De plus, ces cellules présentent plusieurs défauts au niveau de leur recombinaison V(D)J. Ainsi, la mort cellulaire observée chez les cellules progénitrices B de la souris TC-PTP-/- pourrait donc être expliquée par une anomalie au niveau de la recombinaison V(D)J durant le développement des lymphocytes. Ces multiples observations liant TC-PTP à la lymphopoïèse des cellules B ont menées à l'étude de l'implication de la protéine dans le développement de la leucémie. Par conséquent, une étude de cette phosphatase chez les patients atteints de la leucémie aïgue lymphoblastique des cellules B ont été entamés et sont adressés dans cette thèse. Le projet de recherche présenté procure d'importantes informations concernant le rôle de TC-PTP dans le développement du système immunitaire ainsi que sa fonction dans les maladies auto-immunes affectant la population.
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Books on the topic "System immunology"

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Kuby, Janis. Immunology. 2nd ed. New York: W.H. Freeman, 1994.

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Immunology. New York: W.H. Freeman, 1992.

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A, Goldsby Richard, ed. Immunology. 5th ed. New York: W.H. Freeman, 2003.

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Immunology. 3rd ed. New York: W.H. Freeman, 1997.

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Immunology. Oxford: Oxford University Press, 2010.

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1943-, Virella Gabriel, ed. Medical immunology. 5th ed. New York: M. Dekker, 2001.

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Peter, Wood. Understanding immunology. 3rd ed. Harlow, England: Prentice Hall, 2011.

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1948-, Novak Robert, ed. Immunology. Philadelphia: Mosby/Elsevier, 2006.

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Thao, Doan, ed. Immunology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2008.

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R, Green Douglas, ed. Immunology, a synthesis. 2nd ed. Sunderland, Mass: Sinauer Associates, 1991.

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Book chapters on the topic "System immunology"

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M. Silver, Richard, and Stephen Elmore. "Immune system modulators." In Medical Immunology, 335–45. 7th edition. | Boca Raton : Taylor & Francis, 2020.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429278990-24.

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Rathore, Heena. "Immunology and Immune System." In Mapping Biological Systems to Network Systems, 51–65. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29782-8_5.

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Lees, Jason R., Agnes M. Azimzadeh, Yaozhong Ding, Tonya J. Webb, and Jonathan S. Bromberg. "Cells of the immune system." In Transplant Immunology, 25–47. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781119072997.ch2.

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Felippe, M. Julia B. "The Immune System." In Equine Clinical Immunology, 1–10. Chichester, UK: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781119086512.ch01.

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Cruse, Julius M., and Robert E. Lewis. "The Complement System." In Atlas of Immunology, 207–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-11196-3_11.

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Su, Charles A., William M. Baldwin, and Robert L. Fairchild. "Soluble mediators in the immune system." In Transplant Immunology, 48–64. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781119072997.ch3.

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Catania, Louis J. "Immunology." In The Paradox of the Immune System, 181–223. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-95187-6.00001-7.

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Laurell, Anna-Brita. "The complement system." In Immunology, 57–65. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-407-00372-9.50009-2.

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Male, David. "The Immune System." In Immunology, 1–25. 6th ed. CRC Press, 2021. http://dx.doi.org/10.1201/9781003137658-1.

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"The Innate Immune System." In Immunology, 20–40. Chichester, UK: John Wiley & Sons, Ltd, 2011. http://dx.doi.org/10.1002/9781119998648.ch2.

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Conference papers on the topic "System immunology"

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Liu, Tong, and Yazhe Wang. "An Immunology-Based Security System Model for Authorization." In 2015 International Conference on Computational Intelligence and Communication Networks (CICN). IEEE, 2015. http://dx.doi.org/10.1109/cicn.2015.205.

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Dong, WEI, YANG Shou-bao, and LIU Xiao-qian. "Artificial Immunology Based Anti-Pollution P2P File Sharing System." In Sixth International Conference on Grid and Cooperative Computing (GCC 2007). IEEE, 2007. http://dx.doi.org/10.1109/gcc.2007.44.

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Nair, Adarsh G., Sanjeev Agarwal, and K. Krishnamurthy. "Immunology Based Multi-Robot Collaboration for Countermine Operations." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-82707.

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Past studies have shown that mechanisms employed by biological systems can motivate development of algorithms for coordination of distributed systems. In this study, an immune system based collaboration is established between heterogeneous robots to perform countermine operations. Heterogeneity of the robots is defined based on their capabilities to detect and/or mark location of mines, and diffuse them. Concepts related to an immune system like clonal expansion, primary and secondary response, immune memory and antigen specificity are exploited in this study. The developed methodology is validated by simulation studies using MATLAB.
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Tie-Shan ZHAO, Zeng-Zhi Li, Ze-Min WANG, and Xiao-Jun LIN. "An Adaptive LAN Intrusion Detection System Based on Computer Immunology." In 2007 IEEE International Conference on Robotics and Biomimetics (ROBIO '07). IEEE, 2007. http://dx.doi.org/10.1109/robio.2007.4522517.

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Elsadig, Muna, and Azween Abdullah. "Biological inspired approach in parallel immunology system for network security." In 2008 International Symposium on Information Technology. IEEE, 2008. http://dx.doi.org/10.1109/itsim.2008.4631545.

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Qian-mu, Li, Xu Man-wu, and Zhang Hong. "A Root-fault Detection System of Grid Based on Immunology." In 2006 Fifth International Conference on Grid and Cooperative Computing (GCC'06). IEEE, 2006. http://dx.doi.org/10.1109/gcc.2006.17.

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Kolesnikova, S. I., and E. V. Kustova. "Modeling the impact on the stochastic object of immunology." In X All-Russian Scientific Conference "System Synthesis and Applied Synergetics". Southern Federal University, 2023. http://dx.doi.org/10.18522/syssyn-2022-54.

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YuJing and WangFeng. "Strategy research of detectors in Distributed Intrusion Detection system from immunology." In 2013 IEEE Conference Anthology. IEEE, 2013. http://dx.doi.org/10.1109/anthology.2013.6784843.

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Al-Taee, Majid A., Lina Souan, Ali Al-Haj, Ahmed Mohsen, and Zahra J. Muhsin. "Quality Control information system for immunology/ serology tests in medical laboratories." In 2009 6th International Multi-Conference on Systems, Signals and Devices (SSD). IEEE, 2009. http://dx.doi.org/10.1109/ssd.2009.4956820.

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Jiang, Frank, Sai Ho Ling, Kit Yan Chan, Zenon Chaczko, Frank H. F. Leung, and Michael R. Frater. "An immunology-inspired multi-engine anomaly detection system with hybrid particle swarm optimisations." In 2012 IEEE International Conference on Fuzzy Systems (FUZZ-IEEE). IEEE, 2012. http://dx.doi.org/10.1109/fuzz-ieee.2012.6251241.

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Reports on the topic "System immunology"

1

Lee, Peter P. Immunology, Systems Biology, and Immunotherapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada485652.

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Lee, Peter P. Immunology, Systems Biology, and Immunotherapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada532381.

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Lee, Peter P. Immunology, Systems Biology, and Immunotherapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada505203.

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4

Marceau, Carla, Matthew Stillerman, Maureen Stiliman, and Stephanie Forrest. Computational Immunology for the Defense of Large Scale Systems. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407600.

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You might also be interested in the extended bibliographies on the topic 'System immunology' for particular source types:
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