Добірка наукової літератури з теми "Immunity control"

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Статті в журналах з теми "Immunity control"

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Bendelac, Albert, and Douglas T. Fearon. "Innate immunity Innate pathways that control acquired immunity." Current Opinion in Immunology 9, no. 1 (February 1997): 1–3. http://dx.doi.org/10.1016/s0952-7915(97)80151-3.

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Busslinger, M., and A. Tarakhovsky. "Epigenetic Control of Immunity." Cold Spring Harbor Perspectives in Biology 6, no. 6 (June 1, 2014): a019307. http://dx.doi.org/10.1101/cshperspect.a019307.

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Busslinger, M., and A. Tarakhovsky. "Epigenetic Control of Immunity." Cold Spring Harbor Perspectives in Biology 6, no. 7 (July 1, 2014): a024174. http://dx.doi.org/10.1101/cshperspect.a024174.

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Tracey, Kevin J. "Reflex control of immunity." Nature Reviews Immunology 9, no. 6 (June 2009): 418–28. http://dx.doi.org/10.1038/nri2566.

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Gamboa, Lena, Ali H. Zamat, and Gabriel A. Kwong. "Synthetic immunity by remote control." Theranostics 10, no. 8 (2020): 3652–67. http://dx.doi.org/10.7150/thno.41305.

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ALVAREZ, MARÍA E., FLORENCIA NOTA, and DAMIÁN A. CAMBIAGNO. "Epigenetic control of plant immunity." Molecular Plant Pathology 11, no. 4 (June 1, 2010): 563–76. http://dx.doi.org/10.1111/j.1364-3703.2010.00621.x.

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Chen, Huihui, Xiaohan Ning, and Zhengfan Jiang. "Caspases control antiviral innate immunity." Cellular & Molecular Immunology 14, no. 9 (July 10, 2017): 736–47. http://dx.doi.org/10.1038/cmi.2017.44.

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Bachère, Evelyne. "Shrimp immunity and disease control." Aquaculture 191, no. 1-3 (November 2000): 3–11. http://dx.doi.org/10.1016/s0044-8486(00)00413-0.

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Shanker, Anil. "Adaptive control of innate immunity." Immunology Letters 131, no. 2 (July 2010): 107–12. http://dx.doi.org/10.1016/j.imlet.2010.04.002.

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Kiberstis, P. A. "Oncogene control of antitumor immunity." Science 352, no. 6282 (April 7, 2016): 183. http://dx.doi.org/10.1126/science.352.6282.183-d.

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Дисертації з теми "Immunity control"

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Wong, Wing-ki Vicky. "An immunity-based distributed multiagent control framework." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37314348.

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Wong, Wing-ki Vicky, and 黃穎琪. "An immunity-based distributed multiagent control framework." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37314348.

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Meyer, Andrea Michael. "Ro52 in innate immunity, proliferation control and cancer /." Zürich : ETH, 2009. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=18198.

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Booth, Kimberly Katie. "Developmental Effects on Immunity: Hormonal and Proteinase Control." Diss., North Dakota State University, 2016. http://hdl.handle.net/10365/25809.

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Insects are ubiquitous, diverse, and able to combat infections despite their lack of adaptive immunity. Insects have a robust innate immune system that is divided into two branches, cell-mediated and humoral. Activation of cell-mediated immune responses results in phagocytosis, nodule formation, and encapsulation by the insect’s immune cells, hemocytes. Activation of humoral immunity results in the production of anti-microbial peptides (AMPs) and phenoloxidase (PO). Insect immune responses can be plastic with development. However, research on how and why insect immunity changes with age as insects develop within a larval developmental stage (instar) is limited and contradictory. In my dissertation research, I answer two main questions: 1) how do immune responses vary within an instar and 2) what drives changes in immunity within an instar? My dissertation research showed that humoral immune responses are more robust at the beginning of the 5th and final instar in Manduca sexta (tobacco hornworm) compared to responses from animals later within that instar. Many changes occur within an instar that could affect immunity. For example, I found that protein expression of matrix metalloproteinase (MMP) in immune tissues of M. sexta decreases throughout the 5th instar. Though MMPs are involved in immune responses in other insects, MMP was not found to be immunostimulatory in M. sexta. Another important factor that changes within an instar is the level of juvenile hormone (JH). JH, a developmental hormone that prevents early molting, peaks early and decreases within an instar until molting. I determined that JH is necessary to survive an infection, control bacterial growth in hemolymph (insect blood), and mount an AMP activity immune response. My dissertation research has established that there is a development-immunity link, and that the naturally fluctuating levels of JH may mediate the effect of development on immunity.
North Dakota State University Graduate School Doctoral Dissertation Award
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Abdullah, Mohamed Rusli. "Malaria and malaria control in Jeli Peninsular Malaysia." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266047.

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Tkacz, Andrzej. "Plant genotype, immunity and soil composition control the rhizosphere microbiome." Thesis, University of East Anglia, 2013. https://ueaeprints.uea.ac.uk/48113/.

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Three model plant and three crop plant species were grown for three generations in sand and compost. Pots were inoculated with 10 % soil initially, and with 10% of growth medium from the previous generation in generations 2 and 3, keeping replicates separate for all three generations. The microbiome community structure of the plant rhizosphere in each generation was characterised using ARISA DNA fingerprinting and 454 sequencing. Rhizosphere bacterial and fungal communities are different from those in bulk soil and there are also differences in the microbial community between different plant species. Plants both select and suppress specific bacteria and fungi in the rhizosphere microbiome, presumably via composition of their root exudates. Two out of three most abundant bacteria selected in the rhizosphere were isolated. These isolates proved to possess plant growth promotion properties. Plants are able to “farm” the soil in order to enrich it with plant growth promoting rhizobacteria (PGPR) species. However, in some plant species rhizospheres, invasions of opportunists and pathogens take place, mimicking events in plant monocultures. Other experiments using this multi-replicate system allowed for statistical analysis of the influence of Arabidopsis and Medicago mutants on the rhizosphere microbiome. Three groups of Arabidopsis mutants were tested: plants unable to produce aliphatic glucosinolates, plants impaired in the PAMP-triggered immune response and plants unable and over-expressed in methyl halides production and one group of Medicago mutants which are impaired in the mycorrhization ability. All these plant genotypes, except those for methyl-halide production and one genotype involved in PAMP response, significantly altered the rhizosphere microbiome.
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Coss, Samantha Lynn. "T cell immunity and postpartum control of the hepatitis C virus." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1532085655839592.

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Kew, Chun [Verfasser], and Adam [Gutachter] Antebi. "Control of Innate Immunity by RNA Metabolism / Chun Kew ; Gutachter: Adam Antebi." Köln : Universitäts- und Stadtbibliothek Köln, 2018. http://d-nb.info/1180601556/34.

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Lee, Hyun-Hee. "Immunity in the newborn control by IL-13 receptor and dendritic cells /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5939.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.
"May 2007" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.
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Saxena, Pallavi. "Role of Inflammatory Cytokine Signaling in Control of Bacterial Infection." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41076.

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The immune system rapidly mounts an innate immune response to invading pathogens that is accompanied by antigen-presentation, to promote the development of the adaptive immune response. These responses orchestrate through signal transduction by PRRs that recognize PAMPs, which results in the expression of various cytokines and mediators to promote pathogen control. Herein, we investigated the role of the type I interferon (IFN)- and the p38MAPK- pathways in response to infection with Salmonella Typhimurium (ST). We delved into the mechanisms through which IFNAR1-signaling results in host susceptibility against ST and show that while STAT2 and IRF9 promote susceptibility against ST, this is antagonized by STAT1. Our results indicate that IFNAR1-signaling induces IL-10 production through the ISGF3 complex, which indeed inhibits the production of IL-1β (via NLRP3 and caspase-1) resulting in a state of resistance against ST. Furthermore, our work elucidates that MK2, which is a p38MAPK substrate promotes host resistance, which is contradictory to type I IFNs despite the fact that MK2 regulates cytokine expression in a similar pattern to IRF9. We demonstrate that MK2 inhibits inflammasome signaling via NLRP3, caspase-1 and caspase11. We also reveal a role for MK2 in regulating IL-1β production via distinct signaling pathways including inhibition of MSK1/2 besides activation of the autophagic machinery; which also contribute to the enhanced inflammasome activation seen in Mk2- deficient cells. Thus, our observations illuminate the fact that the type I IFN pathway and the p38MAPK pathway are only dependent on each other to a certain extent in modulating the innate immune response to Salmonella infection, thereby bringing about varied outcomes in the infected host.
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Книги з теми "Immunity control"

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C, Cottrell Martha, and Mead Mark N, eds. AIDS, macrobiotics, and natural immunity. Tokyo: Japan Publications, 1990.

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Symposium on Innate Immunity to Pulmonary Infection (2005 University of Cape Town, Medical School). Innate immunity to pulmonary infection. Edited by Chadwick Derek, Goode Jamie, and Novartis Foundation. Chichester: John Wiley, 2006.

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Symposium on Innate Immunity to Pulmonary Infection (2005 University of Cape Town, Medical School). Innate Immunity to Pulmonary Infection. New York: John Wiley & Sons, Ltd., 2007.

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Viral immunity: A 10-step plan to enhance your immunity against viral disease using natural medicines. Charlottesville, VA: Hampton Roads Pub., 2002.

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E, Briles David, ed. Genetic control of the susceptibility to bacterial infection. Berlin: Springer-Verlag, 1986.

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1935-, Greenwood David, ed. Medical microbiology: A guide to microbial infections : pathogenesis, immunity, laboratory diagnosis and control. Edinburgh: Churchill Livingstone/Elsevier, 2007.

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1935-, Greenwood David, Slack Richard C. B, and Peutherer J. F, eds. Medical microbiology: A guide to microbial infections : pathogenesis, immunity, laboratory diagnosis, and control. Edinburgh: Churchill Livingstone, 2002.

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R, Black, ed. Medical microbiology: A guide to microbial infections : pathogenesis : immunity, laboratory diagnosis and control. Edinburgh: Churchill Livingstone, 1990.

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Lane, I. William. Immune power. Garden City Park, NY: Avery Pub. Group, 1999.

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J, Brown Stephen. Host immune response to feeding by ticks: A natural biological control mechanism. Nairobi, Kenya: ICIPE Science Press, International Centre of Insect Physiology and Ecology, 1988.

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Частини книг з теми "Immunity control"

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Saijo, Yusuke, and Eva-Maria Reimer-Michalski. "Epigenetic Control of Plant Immunity." In Epigenetic Memory and Control in Plants, 57–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_4.

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Ceuppens, Jan L., and James S. Goodwin. "Control of Antibody and Autoantibody Production by Prostaglandin E." In Prostaglandins and Immunity, 99–121. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2603-8_5.

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Schmunis, Gabriel A. "Epidemiology, Disease Transmission, Prevention, and Control." In Infection, Resistance, and Immunity, 435–58. Boca Raton: Routledge, 2022. http://dx.doi.org/10.1201/9780203750964-21.

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Katafuchi, Toshihiko, Zhichun Shi, Sachiko Take, and Tetsuro Hori. "Hypothalamo-Sympathetic Control of Cellular Immunity." In Catecholamine Research, 277–80. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3538-3_65.

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Mowbray, J. F., and J. L. Underwood. "Control of Maternal Immunity to Trophoblast." In Reproductive Immunology, 179–86. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4197-0_17.

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Wakelin, D. "Genetic Control of Immunity to Helminths." In Helminthology, 335–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78838-3_15.

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Wakelin, D. "Genetic Control of Immunity to Helminth Infections." In Parasitology in Focus, 651–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-662-09200-2_15.

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Mowbray, James. "Role of Immunity in Control of Fertility." In Natural Human Fertility, 130–34. London: Palgrave Macmillan UK, 1988. http://dx.doi.org/10.1007/978-1-349-09961-0_9.

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Guencheva, G., P. Popova, F. J. McGuigan, and N. Nikolov. "Experimental Stress and Immunity: Past, Present and Future." In Stress and Tension Control 3, 261–80. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-7915-1_28.

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Ryffel, Bernhard, Muazzam Jacobs, Shreemanta Parida, Tania Botha, Dieudonnée Togbe, and Valerie Quesniaux. "Toll-Like Receptors and Control of Mycobacterial Infection in Mice." In Innate Immunity to Pulmonary Infection, 127–41. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035399.ch11.

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Тези доповідей конференцій з теми "Immunity control"

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Varner, Judith A. "Abstract IA19: PI3Kgamma control of antitumor immunity." In Abstracts: AACR Special Conference on Targeting PI3K/mTOR Signaling; November 30-December 8, 2018; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.pi3k-mtor18-ia19.

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Rychkov, E., and V. Patyukov. "Troposphere communication systems noise-immunity estimation." In 2013 International Siberian Conference on Control and Communications (SIBCON 2013). IEEE, 2013. http://dx.doi.org/10.1109/sibcon.2013.6693648.

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Michel, Kristin. "The regulation of humoral control immunity in mosquitoes." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92697.

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Lu, Binxian, Wei Zhang, and Zezhong Wang. "Research of Conduction Immunity of Control Shielded Cable." In 2009 Asia-Pacific Power and Energy Engineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/appeec.2009.4918664.

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Merad, Miriam. "Abstract IA19: Myeloid cell control of tumor immunity." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-ia19.

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Jiang, J., and R. Cook. "A Fast Parameter Tracking RLS Algorithm with High Noise Immunity." In 1993 American Control Conference. IEEE, 1993. http://dx.doi.org/10.23919/acc.1993.4793300.

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Perez, Andres E., Hever Moncayo, Israel Moguel, Mario G. Perhinschi, Dia Al Azzawi, and Adil Togayev. "Development of Immunity Based Adaptive Control Laws for Aircraft Fault Tolerance." In ASME 2014 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/dscc2014-5890.

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This paper presents the development and testing of a novel fault tolerant adaptive control system based on a bio-inspired immunity-based mechanism applied to an aircraft fighter model. The proposed baseline control laws use a non-linear dynamic inversion and model reference adaptive control on the inner loops of the aircraft dynamics. In this new approach, the baseline controllers are augmented with an artificial immune system mechanism that relies on a direct compensation inspired primarily by the biological immune system response. The effectiveness of the approach is demonstrated through a full 6 degrees-of-freedom aircraft model interfaced with a Flight gear environment. The performance of the proposed control laws are investigated under a novel set of performance metrics, which quantify the level of input activity from the pilot and from the control surfaces in order to ensure the stability and performance of the aircraft under different actuator and structural failures. Optimization of the parameters of the artificial immunity system is performed using a genetic algorithm. The results show that the optimized fault tolerant adaptive control laws improve significantly the failure rejection using minimum pilot input and control surfaces activity under upset flight conditions.
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Tan, Xiaojun, Conggang Zhang, and Zhijian J. Chen. "Abstract A116: Lipid control of DNA-stimulated innate immunity." 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-a116.

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Zharinov, Igor, Danil Zakoldaev, Anatoly Shukalov, and Oleg Zharinov. "The technological environment cyber-physical system noise immunity control." In PROCEEDINGS OF THE II INTERNATIONAL CONFERENCE ON ADVANCES IN MATERIALS, SYSTEMS AND TECHNOLOGIES: (CAMSTech-II 2021). AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0092427.

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Li, He, Hong Li, Shu Jun Tan, and Lei Wang. "Coal Mining Automatic Control Equipment Surge Immunity Test Analysis." In 2023 5th International Conference on Intelligent Control, Measurement and Signal Processing (ICMSP). IEEE, 2023. http://dx.doi.org/10.1109/icmsp58539.2023.10171102.

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Звіти організацій з теми "Immunity control"

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Lillehoj, Hyun, Dan Heller, and Mark Jenkins. Cellular and molecular identification of Eimeria Acervulina Merozoite Antigens eliciting protective immunity. United States Department of Agriculture, November 1992. http://dx.doi.org/10.32747/1992.7561056.bard.

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Coccidiosis, ubiquitous diseases of poultry, seriously impair the growth and feed utilization of livestock and poultry. Coccidiosis causes over $600 million annual losses world-wide and no vaccine is currently available. The goal of this study was to investigate the cellular and molecular mechanisms controlling protective immune responses to coccidia parasites in order to develop immunological control strategy against coccidiosis. The major findings of this study were: 1) cell-mediated immunity plays a major role in protection against coccidiosis, 2) when different genetic lines showing different levels of disease susceptibility were compared, higher T-cell response was seen in the strains of chickens showing higher disease resistance, 3) early interferon secretion was observed in more coccidia-resistant chicken strains, 4) both sporozoite and merozoite antigens were able to induce interferon production, and 5) chicken monoclonal antibodies which detect immunogenic coccidia proteins have been developed. This study provided a good background work for future studies toward the development of recombinant coccidial vaccine. Availability of chicken monoclonal antibodies which detect immunogenic coccidia proteins will enhance our ability to identify potential coccidial vaccine antigens.
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, July 2004. http://dx.doi.org/10.32747/2004.7587236.bard.

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Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.
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3

Sessa, Guido, and Gregory Martin. role of FLS3 and BSK830 in pattern-triggered immunity in tomato. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604270.bard.

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Анотація:
Pattern-recognition receptors (PRRs) located on the plant cell surface initiate immune responses by perceiving conserved pathogen molecules known as pathogen-associated molecular patterns (PAMPs). PRRs typically function in multiprotein complexes that include transmembrane and cytoplasmickinases and contribute to the initiation and signaling of pattern-triggered immunity (PTI). An important challenge is to identify molecular components of PRR complexes and downstream signaling pathways, and to understand the molecular mechanisms that mediate their function. In research activities supported by BARD-4931, we studied the role of the FLAGELLIN SENSING 3 (FLS3) PRR in the response of tomato leaves to flagellin-derivedPAMPs and PTI. In addition, we investigated molecular properties of the tomato brassinosteroid signaling kinase 830 (BSK830) that physically interacts with FLS3 and is a candidate for acting in the FLS3 signaling pathway. Our investigation refers to the proposal original objectives that were to: 1) Investigate the role of FLS3 and its interacting proteins in PTI; 2) Investigate the role of BSK830 in PTI; 3) Examine molecular and phosphorylation dynamics of the FLS3-BSK830 interaction; 4) Examine the possible interaction of FLS3 and BSK830 with Pstand Xcveffectors. We used CRISPR/Cas9 techniques to develop plants carrying single or combined mutations in the FLS3 gene and in the paralogsFLS2.1 and FLS2.2 genes, which encode the receptor FLAGELLIN SENSING2 (FLS2), and analyzed their function in PTI. Domain swapping analysis of the FLS2 and FLS3 receptors revealed domains of the proteins responsible for PAMP detection and for the different ROS response initiated by flgII-28/FLS3 as compared to flg22/FLS2. In addition, in vitro kinase assays and point mutations analysis identified FLS2 and FLS3 domains required for kinase activity and ATP binding. In research activities on tomato BSK830, we found that it interacts with PRRs and with the co-receptor SERK3A and PAMP treatment affects part of these interactions. CRISPR/Cas9 bsk830 mutant plants displayed enhanced pathogen susceptibility and reduced ROS production upon PAMP treatment. In addition, BSK830 interacted with 8 Xanthomonastype III secreted effectors. Follow up analysis revealed that among these effectors XopAE is part of an operon, is translocated into plant cells, and displays E3 ubiquitinligase activity. Our investigation was also extended to other Arabidopsis and tomato BSK family members. Arabidopsis BSK5 localized to the plant cell periphery, interacted with receptor-like kinases, and it was phosphorylatedin vitro by the PEPR1 and EFRPRRs. bsk5 mutant plants displayed enhanced susceptibility to pathogens and were impaired in several, but not all, PAMP-induced responses. Conversely, BSK5 overexpression conferred enhanced disease resistance and caused stronger PTI responses. Genetic complementation suggested that proper localization, kinase activity, and phosphorylation by PRRs are critical for BSK5 function. BSK7 and BSK8 specifically interacted with the FLS2 PRR, their respective mutant plants were more susceptible to B. cinereaand displayed reduced flg22-induced responses. The tomato BSK Mai1 was found to interact with the M3KMAPKKK, which is involved in activation of cell death associated with effector-triggered immunity. Silencing of Mai1 in N. benthamianaplants compromised cell death induced by a specific class of immune receptors. In addition, co-expression of Mai1 and M3Kin leaves enhanced MAPKphosphorylation and cell death, suggesting that Mai1 acts as a molecular link between pathogen recognition and MAPK signaling. Finally, We identified the PP2C phosphatase Pic1 that acts as a negative regulator of PTI by interacting with and dephosphorylating the receptor-like cytoplasmickinase Pti1, which is a positive regulator of plant immunity. The results of this investigation shed new light on the molecular characteristics and interactions of components of the immune system of crop plants providing new knowledge and tools for development of novel strategies for disease control.
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4

Avni, Adi, and Gitta L. Coaker. Proteomic investigation of a tomato receptor like protein recognizing fungal pathogens. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600030.bard.

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Анотація:
Maximizing food production with minimal negative effects on the environment remains a long-term challenge for sustainable food production. Microbial pathogens cause devastating diseases, minimizing crop losses by controlling plant diseases can contribute significantly to this goal. All plants possess an innate immune system that is activated after recognition of microbial-derived molecules. The fungal protein Eix induces defense responses in tomato and tobacco. Plants recognize Eix through a leucine-rich-repeat receptor- like-protein (LRR-RLP) termed LeEix. Despite the knowledge obtained from studies on tomato, relatively little is known about signaling initiated by RLP-type immune receptors. The focus of this grant proposal is to generate a foundational understanding of how the tomato xylanase receptor LeEix2 signals to confer defense responses. LeEix2 recognition results in pattern triggered immunity (PTI). The grant has two main aims: (1) Isolate the LeEix2 protein complex in an active and resting state; (2) Examine the biological function of the identified proteins in relation to LeEix2 signaling upon perception of the xylanase elicitor Eix. We used two separate approaches to isolate receptor interacting proteins. Transgenic tomato plants expressing LeEix2 fused to the GFP tag were used to identify complex components at a resting and activated state. LeEix2 complexes were purified by mass spectrometry and associated proteins identified by mass spectrometry. We identified novel proteins that interact with LeEix receptor by proteomics analysis. We identified two dynamin related proteins (DRPs), a coiled coil – nucleotide binding site leucine rich repeat (SlNRC4a) protein. In the second approach we used the split ubiquitin yeast two hybrid (Y2H) screen system to identified receptor-like protein kinase At5g24010-like (SlRLK-like) (Solyc01g094920.2.1) as an interactor of LeEIX2. We examined the role of SlNRC4a in plant immunity. Co-immunoprecipitation demonstrates that SlNRC4a is able to associate with different PRRs. Physiological assays with specific elicitors revealed that SlNRC4a generally alters PRR-mediated responses. SlNRC4a overexpression enhances defense responses while silencing SlNRC4 reduces plant immunity. We propose that SlNRC4a acts as a non-canonical positive regulator of immunity mediated by diverse PRRs. Thus, SlNRC4a could link both intracellular and extracellular immune perception. SlDRP2A localizes at the plasma membrane. Overexpression of SlDRP2A increases the sub-population of LeEIX2 inVHAa1 endosomes, and enhances LeEIX2- and FLS2-mediated defense. The effect of SlDRP2A on induction of plant immunity highlights the importance of endomembrane components and endocytosis in signal propagation during plant immune . The interaction of LeEIX2 with SlRLK-like was verified using co- immunoprecipitation and a bimolecular fluorescence complementation assay. The defence responses induced by EIX were markedly reduced when SlRLK-like was over-expressed, and mutation of slrlk-likeusing CRISPR/Cas9 increased EIX- induced ethylene production and SlACSgene expression in tomato. Co-expression of SlRLK-like with different RLPs and RLKs led to their degradation, apparently through an endoplasmic reticulum-associated degradation process. We provided new knowledge and expertise relevant to expression of specific be exploited to enhance immunity in crops enabling the development of novel environmentally friendly disease control strategies.
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5

Montville, Thomas J., and Roni Shapira. Molecular Engineering of Pediocin A to Establish Structure/Function Relationships for Mechanistic Control of Foodborne Pathogens. United States Department of Agriculture, August 1993. http://dx.doi.org/10.32747/1993.7568088.bard.

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This project relates the structure of the bacteriocin molecule (which is genetically determined) to its antimicrobial function. We have sequenced the 19,542 bp pediocin plasmid pMD136 and developed a genetic transfer system for pediococci. The pediocin A operon is complex, containing putative structural, immunity, processing, and transport genes. The deduced sequence of the pediocin A molecule contains 44 amino acids and has a predicted PI of 9.45. Mechanistic studies compared the interaction of pediocin PA-1 and nisin with Listeria monocytgenes cells and model lipid systems. While significant nisin-induced intracellular ATP depletion is caused by efflux, pediocin-induced depletion is caused exclusively by hydrolysis. Liposomes derived from L. monocytogenes phospholipids were used to study the physical chemistry of pediocin and nisin interactions with lipids. Their different pH optima are the results of different specific ionizable amino acids. We generated a predicted 3-D structural model for pediocin PA-1 and used a variety of mutant pediocins to demonstrate that the "positive patch" at residues 11 and 12 (and not the YGNGV consensus sequence) is responsible for the binding step of pediocin action. This structure/function understanding gained here provides necessary prerequisites to the more efficacious use of bacteriocins to control foodborne pathogens.
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6

Chejanovsky, Nor, and Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592113.bard.

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Анотація:
The restricted host range of many baculoviruses, highly pathogenic to Lepidoptera and non-pathogenic to mammals, limits their use to single or few closely related Lepidopteran species and is an obstacle to extending their implementation for pest control. The insect immune response is a major determinant of the ability of an insect pathogen to efficiently multiply and propagate. We have developed an original model system to study the Lepidopteran antiviral immune response based on Spodoptera littoralis resistance to AcMNPV (Autographa californica multiple nucleopolyhedrovirus) infection and the fascinating immunosuppressive activity of polydnaviruses .Our aim is to elucidate the mechanisms through which the immunosuppressive insect polydnaviruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication. In this study we : 1- Assessed the extent to which and the mechanisms whereby the immunosuppressive Campoletis sonorensis polydnavirus (CsV) or its genes enhanced replication of a well-characterized pathogenic baculovirus AcMNPV, in polydnavirus-immunosuppressedH. zea and S. littoralis insects and S. littoralis cells, hosts that are mildly or non-permissive to AcMNPV. 2- Identified CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). We showed that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen, the baculovirus AcMNPV, to infect the pest. 3. For the first time two PDV-specific genes of the vankyrin and cystein rich-motif families involved in immunosuppression of the host, namely Pvank1 and Hv1.1 respectively, enhanced the efficacy of an insect pathogen toward a semipermissive pest. 4. Pvank1 inhibits apoptosis of Spodopteran cells elucidating one functional aspect of PDVvankyrins. 5. That Pvank-1 and Hv1.1 do not show cooperative effect in S. littoralis when co-expressed during AcMNPV infection. Our results pave the way to developing novel means for pest control, including baculoviruses, that rely upon suppressing host immune systems by strategically weakening insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence. Also, we expect that the above result will help to develop systems for enhanced insect control that may ultimately help to reduce transmission of insect vectored diseases of humans, animals and plants as well as provide mechanisms for suppression of insect populations that damage crop plants by direct feeding.
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7

McElwain, Terry F., Eugene Pipano, Guy H. Palmer, Varda Shkap, Stephn A. Hines, and Wendy C. Brown. Protection of Cattle against Babesiosis: Immunization against Babesia bovis with an Optimized RAP-1/Apical Complex Construct. United States Department of Agriculture, September 1999. http://dx.doi.org/10.32747/1999.7573063.bard.

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Анотація:
Previous research and current efforts at control of babesiosis fall short of meeting the needs of countries where the disease is endemic, such as Israel, as well as the needs of exporting countries and countries bordering on endemic areas, such as the U.S. Our long-term goal is to develop improved methods of immunization against bovine babesiosis based on an understanding of the molecular mechanisms of immune protection and parasite targets of a protective immune response. In our previous BARD project, we established the basis for focusing on rhoptry antigens as components of a subunit vaccine against bovine babesiosis, and for additional research to better characterize rhoptry associated protein-1 (RAP-1) as a target of protective immunity. In this continuation BARD project, our objectives were to [1] optimize the immune response against RAP-1, and [2] identify additional rhoptry candidate vaccine antigens. The entire locus encoding B. bovis RAP-1 was sequenced, and the rap-1 open reading frame compared among several strains. Unlike B. bigemina, in which multiple gene copies with variant domains encode RAP-1, the B. bovis RAP-1 locus contains only two identical genes which are conserved among strains. Through testing of multiple truncated constructs of rRAP-1, one or more immunodominant T cell epitopes were mapped to the amino terminal half of RAP-1. At least one linear and one conformational B cell epitope have been demonstrated in the same amino terminal construct, which in B. bigemina RAP-1 also contains an epitope recognized by neutralizing antibody. The amine terminal half of the molecule represents the most highly conserved part of the gene family and contains motifs conserved broadly among the apicomplexa. In contrast, the carboxy terminal half of B. bovis RAP-1 is less well conserved and contains multiple repeats encoding a linear B cell epitope potentially capable of inducing an ineffective, T cell independent, type 2 immune response. Therefore, we are testing an amino terminal fragment of RAP-1 (RAP-1N) in an immunization trial in cattle. Cattle have beer immunized with RAP-1N or control antigen, and IL-12 with Ribi adjuvant. Evaluation of the immune response is ongoing, and challenge with virulent B. bovis will occur in the near future. While no new rhoptry antigens were identified, our studies did identify and characterize a new spherical body antigen (SBP3), and several heat shock proteins (HSP's). The SBP3 and HSP21 antigens stimulate T cells from immune cattle and are considered new vaccine candidates worthy of further testing. Overall, we conclude that a single RAP-1 vaccine construct representing the conserved amino terminal region of the molecule should be sufficient for immunization against all strains of B. bovis. While results of the ongoing immunization trial will direct our next research steps, results at this time are consistent with our long term goal of designing a subunit vaccine which contains only the epitopes relevant to induction of protective immunity. Parallel studies are defining the mechanisms of protective immunity. Apicomplexan protozoa, including babesiosis and malaria, cause persistent diseases for which control is inadequate. The apical organelles are defining features of these complex protozoa, and have been conserved through the evolutionary process, Past and current BARD projects on babesiosis have established the validity and potential of exploiting these conserved organelles in developing improved control methods applicable to all apicomplexan diseases.
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8

Sessa, Guido, та Gregory Martin. MAP kinase cascades activated by SlMAPKKKε and their involvement in tomato resistance to bacterial pathogens. United States Department of Agriculture, січень 2012. http://dx.doi.org/10.32747/2012.7699834.bard.

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Анотація:
The research problem: Pseudomonas syringae pv. tomato (Pst) and Xanthomonas campestrispv. vesicatoria (Xcv) are the causal agents of tomato bacterial speck and spot diseases, respectively. These pathogens colonize the aerial parts of the plant and cause economically important losses to tomato yield worldwide. Control of speck and spot diseases by cultural practices or chemicals is not effective and genetic sources of resistance are very limited. In previous research supported by BARD, by gene expression profiling we identified signaling components involved in resistance to Xcvstrains. Follow up experiments revealed that a tomato gene encoding a MAP kinase kinase kinase (MAPKKKe) is required for resistance to Xcvand Pststrains. Goals: Central goal of this research was to investigate the molecular mechanisms by which MAPKKKεand associated MAP kinase cascades regulate host resistance. Specific objectives were to: 1. Determine whether MAPKKKεplays a broad role in defense signaling in plants; 2. Identify components of MAP kinase cascades acting downstream of MAPKKKε; 3. Determine the role of phosphorylation-related events in the function of MAPKKKε; 4. Isolate proteins directly activated by MAPKKKε-associatedMAPK modules. Our main achievements during this research program are in the following major areas: 1. Characterization of MAPKKKεas a positive regulator of cell death and dissection of downstream MAP kinase cascades (Melech-Bonfil et al., 2010; Melech-Bonfil and Sessa, 2011). The MAPKKKεgene was found to be required for tomato resistance to Xcvand Pstbacterial strains and for hypersensitive response cell death triggered by different R gene/effector gene pairs. In addition, overexpression analysis demonstrated that MAPKKKεis a positive regulator of cell death, whose activity depends on an intact kinase catalytic domain. Epistatic experiments delineated a signaling cascade downstream of MAPKKKεand identified SIPKK as a negative regulator of MAPKKKε-mediated cell death. Finally, genes encoding MAP kinase components downstream of MAPKKKεwere shown to contribute to tomato resistance to Xcv. 2. Identification of tomato proteins that interact with MAPKKKεand play a role in plant immunity (Oh et al., 2011). We identified proteins that interact with MAPKKKε. Among them, the 14-3-3 protein TFT7 was required for cell death mediated by several R proteins. In addition, TFT7 interacted with the MAPKK SlMKK2 and formed homodimersin vivo. Thus, TFT7 is proposed to recruit SlMKK2 and MAPKKK client proteins for efficient signal transfer. 3. Development of a chemical genetic approach to identify substrates of MAPKKKε-activated MAP kinase cascades (Salomon et al., 2009, 2011). This approach is based on engineering the kinase of interest to accept unnatural ATP analogs. For its implementation to identify substrates of MAPKKKε-activated MAP kinase modules, we sensitized the tomato MAP kinase SlMPK3 to ATP analogs and verified its ability to use them as phosphodonors. By using the sensitized SlMPK3 and radiolabeled N6(benzyl)ATP it should be possible to tag direct substrates of this kinase. 4. Development of methods to study immunity triggered by pathogen-associated molecular patterns (PAMPs) in tomato and N. benthamiana plants (Kim et al., 2009; Nguyen et al. 2010). We developed protocols for measuring various PTI-associatedphenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition at the cell wall, activation of MAP kinases, and a luciferase-based reporter system for use in protoplasts. Scientific and agricultural significance: Our research activities discovered and characterized a signal transduction pathway mediating plant immunity to bacterial pathogens. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease. In addition, we successfully developed new biochemical and molecular methods that can be implemented in the study of plant immunity and other aspects of plant biology.
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9

Brayton, Kelly A., Varda Shkap, Guy H. Palmer, Wendy C. Brown, and Thea Molad. Control of Bovine Anaplasmosis: Protective Capacity of the MSP2 Allelic Repertoire. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699838.bard.

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Анотація:
Anaplasmosis is an arthropod-borne disease of cattle caused by the rickettsia Anaplasmamarginale and is an impediment to efficient production of healthy livestock in both Israel and the United States. Currently, the only effective vaccines are derived from the blood of infected cattle. The risk of widespread transmission of both known and newly emergent pathogens has prevented licensure of live blood-based vaccines in the U.S. and is a major concern for their continued use in Israel. Consequently, development of a safe, effective vaccine is a high priority. Despite its drawbacks as a live, blood-based vaccine, the Israel vaccine strain protects against disease upon challenge with wild-type A. marginale in extensive experimental trials and during 50 years of deployment in Israel. Field studies in Australia and Argentina indicate that this protection is broadly effective. Thus, to identify antigens for development of a safe and effective recombinant vaccine, we have used a comparative genomics approach by sequencing the Israel vaccine strain and searching for shared surface antigens with sequenced wild-type U.S. strains. We have focused on Msp2, the immune-dominant but antigenically variable surface protein, based on shared structure among strains and demonstration that antibody from cattle immunized with the Israel vaccine strain binds Msp2 from the genetically and geographically distinct U.S. St. Maries strain, consistent with the ability to protect against St. Maries challenge. Importantly, we have defined the full repertoire of Msp2 simple variants encoded by the vaccine strain and hypothesize that a recombinant vaccine encoding this full repertoire will induce protection equivalent to that induced by the live vaccine strain. Any escape from immunity by generation of complex Msp2 variants is predicted to carry a severe fitness cost that prevents high-level bacteremia and disease— consistent with the type of protection induced by the live vaccine strain. We tested the hypothesis that the Msp2 simple variant repertoires in wild-type A. marginale strains are recognized by antibody from cattle immunized with the Israel vaccine strain and that immunization with the vaccine strain Msp2 repertoire can recapitulate the protection provided by the vaccine strain upon challenge with Israel and U.S. strains of A. marginale. Our findings demonstrate that a set of conserved outer membrane proteins are recognized by immune serum from A. centrale vaccinated animals but that this set of proteins does not include Msp2. These findings suggest that “subdominant” immunogens are required for vaccine induced protection.
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10

Knowles, Donald, and Monica Leszkowicz Mazuz. Transfected Babesia bovis expressing the anti-tick Bm86 antigen as a vaccine to limit tick infestation and protect against virulent challenge. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598160.bard.

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Анотація:
Bovine babesiosis, caused by the apicomplexan parasites Babesiabovisand B. bigemina, is a major tick borne disease of cattle with significant economic importance globally. The vectors of Babesia parasites are R. (Boophilus) annulatusand R. microplus. In Israel these parasites are transmitted manly by R. annulatus. The main goal of the proposal was developing and testing a novel B. bovisvaccine based on stably transfected attenuated B. bovisexpressing the anti-tick Bm86 antigen. This required generating a transfected- attenuated B. bovisparasite containing a bidirectional promoter expressing both, the gfp- bsd selectable marker and the tick vaccine antigen Bm86. The vaccine was tested for its ability to elicit protective immune responses against T. annulatusticks. Efficient control of babesiosis is based on a complex scheme of integrated management, including preventive immunization, anti-babesial chemotherapy and control of tick populations. Live vaccines based on attenuated parasites are the most effective measure to control babesiosis, and are currently used in several countries, including Israel. Live attenuated parasites lead to a chronic infection and development of strong and long term immunity in vaccinated cattle. Still, live vaccines have several limitations, including the difficulty to distinguish among vaccinated and naturally infected cattle and potential for sporadic outbreaks in vaccinated animals. Tick limitation is essential to control babesiosis but the main measure to reduce tick infestation is traditionally approached using acaricides, which is limited by environmental concerns and the development of resistance by the ticks. Alternative tick-control measures including the use of anti-tick vaccines are emerging, and at least partial protective immunity has been achieved against tick vectors by vaccination with recombinant protective tick antigens (ie: Bm86). In addition, the Babesia vaccine development toolbox has been recently expanded with the development of transfection technology in Babesia parasites. In this approved proposal we successfully developed a Babesia live attenuated transfected vaccine, which is able to express a B. bovisMSA-1 signal-Bm86 chimera and eGFP genes under the control of the B. bovisef- 1 and actin promoters respectively. Genetic analysis demonstrated specific stable integration of the transfected genes in the expected ef-1 locus, and immunofluorescence analysis confirmed expression of Bm86 in the surface of transfected parasites. When applied to splenectomized calves, the transfected parasites were able to cause persistent B. bovisinfection with production of antibodies reactive with Bm86 for at least six months. In addition, partial protection against ticks was also observed upon challenging the vaccinated animals with R. annulatuslarvae. However, when used on intact calves, the vaccine failed to elicit detectable immune responses against Bm86, and we are still in the process of interpreting the data and make necessary changes in our experimental approaches. Overall, the results obtained here represent a step forward towards the development of integrated vaccines against both ticks and tick –borne pathogens, using the Babesia attenuated parasites as a platform to the delivery of exogenous protective antigens
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