Relevant bibliographies by topics / Molecular immunity

Contents

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

Academic literature on the topic 'Molecular immunity'

Author: Grafiati
Published: 19 February 2023

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Journal articles on the topic "Molecular immunity"

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Weiss, R. "Maternal Immunity via Molecular Ferry." Science News 135, no. 2 (January 14, 1989): 20. http://dx.doi.org/10.2307/3973428.

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Toka, Felix N., Christopher D. Pack, and Barry T. Rouse. "Molecular adjuvants for mucosal immunity." Immunological Reviews 199, no. 1 (June 2004): 100–112. http://dx.doi.org/10.1111/j.0105-2896.2004.0147.x.

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Blank, Miri, Ori Barzilai, and Yehuda Shoenfeld. "Molecular mimicry and auto-immunity." Clinical Reviews in Allergy & Immunology 32, no. 1 (February 2007): 111–18. http://dx.doi.org/10.1007/s12016-007-0025-8.

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Chan, Siew Leong, Lieh Yoon Low, Simon Hsu, Sheng Li, Tong Liu, Eugenio Santelli, Gaelle Le Negrate, John C. Reed, Virgil L. Woods, and Jaime Pascual. "Molecular Mimicry in Innate Immunity." Journal of Biological Chemistry 284, no. 32 (June 17, 2009): 21386–92. http://dx.doi.org/10.1074/jbc.c109.007591.

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Ulevitch, Richard J. "Molecular Mechanisms of Innate Immunity." Immunologic Research 21, no. 2-3 (2000): 49–54. http://dx.doi.org/10.1385/ir:21:2-3:49.

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Blank, Miri, Ori Barzilai, and Yehuda Shoenfeld. "Molecular mimicry and auto-immunity." Clinical Reviews in Allergy & Immunology 32, no. 1 (February 2007): 111–18. http://dx.doi.org/10.1007/bf02686087.

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Ip, Y. Tony, and Michael Levine. "Molecular genetics of Drosophila immunity." Current Opinion in Genetics & Development 4, no. 5 (October 1994): 672–77. http://dx.doi.org/10.1016/0959-437x(94)90133-n.

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Wu, Hao, and Joseph R. Arron. "TRAF6, a molecular bridge spanning adaptive immunity, innate immunity and osteoimmunology." BioEssays 25, no. 11 (October 17, 2003): 1096–105. http://dx.doi.org/10.1002/bies.10352.

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Pavlov, Valentin A., Sangeeta S. Chavan, and Kevin J. Tracey. "Molecular and Functional Neuroscience in Immunity." Annual Review of Immunology 36, no. 1 (April 26, 2018): 783–812. http://dx.doi.org/10.1146/annurev-immunol-042617-053158.

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Goncharova, Larisa B., and Alexander O. Tarakanov. "Molecular networks of brain and immunity." Brain Research Reviews 55, no. 1 (August 2007): 155–66. http://dx.doi.org/10.1016/j.brainresrev.2007.02.003.

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Dissertations / Theses on the topic "Molecular immunity"

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Steele, John. "Molecular recognition in plant immunity." Thesis, University of East Anglia, 2016. https://ueaeprints.uea.ac.uk/58564/.

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Plant pathogens constitute a major threat to global food security. The use of naturally resistant crop varieties can limit crop losses, however new races of pathogen can arise that are able to overcome these defences. Plant breeding for race-specific resistance typically relies on disease-resistance genes, which generally encode proteins with nucleotide-binding and leucine-rich repeat domains (NB-LRRs). NB-LRRs are a large of proteins found in both plants and animals, with plant NB-LRRs further classified by the presence of N-terminal coiled-coil or toll-interleukin receptor domains. Although qualitative models exist to describe R-protein regulation and activation, these are predominantly based on genetic and molecular studies. Biochemical investigations into R-protein function have been hampered by difficulties obtaining sufficient yields of material. When suitable material has been identified, biochemical studies have been used to complement well-established in planta assays to validate numerous hypotheses. This work describes the screening processes undertaken to obtain R-protein domains suitable for downstream experiments. Using E. coli for high-throughput screening of constructs from a single R-protein, traditional construct design to investigate multiple R-protein domains and expanding our expression hosts to eukaryotic systems we successfully purified four coiled-coil domains and a single NBARC domain for use in downstream experiments. Characterisation of this NBARC domain by circular dichroism and small-angle X-ray scattering indicates that the protein is well-folded and stable in solution, allowing in vitro investigations. In testing models for R-protein regulation we were able to confirm previous findings, such as low levels of ATPase activity, however we were unable to find evidence for a commonly cited method of signal repression. A preliminary crystal structure of the NBARC domain shows significant similarity to Apaf-1, and highlights the importance of conserved motifs in NBARC architecture. The tools presented here should prove a valuable resource to complement existing models to better understand the structure, biochemistry, and ultimately regulation of plant R-proteins.
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Argyriou, Catherine. "Enhanced immunity in Mclk1 +/- mice." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=117161.

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MCLK1 (a.k.a. COQ7) is an evolutionarily conserved mitochondrial hydroxylase necessary ubiquinone biosynthesis. Mclk1+/- mice display a 50% reduction in this protein, as well as an array of phenotypes including increased longevity, decreased ubiquinone in the inner mitochondrial membrane, decreased mitochondrial respiration, and increased mitochondrial oxidative stress. We report here by various measures that Mclk1+/- mutants also exhibit an enhanced immune response in vivo. That is, Mclk1+/- mice mount a more extreme inflammatory response to bacterial lipopolysaccharide stimulation and bacterial infection, evidenced by increased measures of plasma cytokine levels. These mice also demonstrate resilience to tumour development, evidenced by a prolonged, dose-dependent delay in tumour onset following tumour cell xenograft. Furthermore, we report that Mclk1+/- mice react differently than wild-type mice following rapamycin injection. That is, circulating cytokine levels are attenuated in mutants but increased in wild-type mice following rapamycin administration. Despite their more extreme immune response, we demonstrate that Mclk1+/- mutants sustain less tissue damage as a result of infection or old age. Finally, using mouse models of high mitochondrial or cytoplasmic oxidative stress, we report that the Mclk1+/- phenotype is not simply due to increased reactive oxygen species in the mitochondria. These findings suggest characteristics that may contribute to the increased lifespan of these mice, though the causes of these characteristics require further investigation.
MCLK1 (COQ7) est une enzyme hydroxylase conservée au cours de l'évolution et nécessaire pour la biosynthèse de l'ubiquinone. Les souris Mclk1+/- présentent une réduction de 50% du niveau de cette protéine, ainsi qu'une gamme de phénotypes, tels qu'un accroissement de la longévité, une réduction de la quantité d'ubiquinone dans la membrane interne mitochondriale, une réduction de la respiration mitochondriale, et une augmentation du stress oxydatif mitochondrial. Différentes mesures ont démontrées que les souris Mclk1+/- arborent également une meilleure réponse immunitaire suite à la stimulation par des lipopolysaccharides bactériens (LPS) ainsi que par l'infection bactérienne, comme en témoigne une augmentation du niveau de plusieurs cytokines plasmatiques en réponse à ces stimulations. Les mutants Mclk1+/- sont aussi plus résistants au développement de tumeurs, comme en témoigne le délai dans l'apparition de tumeurs après une xénogreffe de cellules tumorales. En outre, nous avons découvert que les souris Mclk1+/- réagissent différemment par rapport aux souris de type sauvage à un traitement avec la rapamycine. Nous avons observé que suite à l'administration prolongée de rapamycine suivi par une injection de LPS, le niveau de cytokines circulantes diminue chez les souris mutantes alors que chez les souris de type sauvage ce niveau augmente. Malgré leur réponse immunitaire plus intense, nous avons démontré que les souris Mclk1+/- subissent moins de dommages tissulaires à la suite d'une infection ou du processus de vieillissement. Enfin, en utilisant des modèles murins de stress oxydatif mitochondrial ou cytoplasmique augmenté, nous avons aussi établi que le phénotype Mclk1+/- ne résulte pas simplement de l'augmentation des radicaux libres dans les mitochondries.
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Wlasiuk, Battagliotti Gabriela. "THE MOLECULAR EVOLUTION OF INNATE IMMUNITY GENES." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195184.

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It is not clear whether genes of the innate immune system of vertebrates are subject to the same selective pressures as genes of the adaptive immune system, despite the fact that innate immunity genes lie directly at the interface between host and pathogens. The lack of consensus about the incidence, type, and strength of selection acting on vertebrate innate immunity genes motivated this study. The goal of this work was to elucidate the general principles of innate immune receptor evolution within and between species. A phylogenetic analysis of the Toll-like receptor 5 (TLR5) in primates showed an excess of nonsynonymous substitutions at certain codons, a pattern that is consistent with recurrent positive selection. The putative sites under selection often displayed radical substitutions, independent parallel changes, and were located in functionally important regions of the protein. In contrast with this interspecific pattern, population genetic analysis of this gene in humans and chimpanzees did not provide conclusive evidence of recent selection. The frequency and distribution of a TLR5 null mutation in human populations further suggested that TLR5 function might be partially redundant in the human immune system (Appendix A). Comparable analyses of the remaining nine human TLRs produced similar results and further pointed to a biologically meaningful difference in the pattern of molecular evolution between TLRs specialized in the recognition of viral nucleic acids and the other TLRs (Appendix B). The general picture that emerges from these studies challenges the conventional idea that pattern recognition receptors are subject to an extreme degree of functional constraint dictated by the recognition of molecules that are essential for microbial fitness. Instead, TLRs display patterns of substitution between species that reflect an old history of positive selection in primates. A common theme, however, is that only a restricted proportion of sites is under positive selection, indicating an equally important role for purifying selection as a conservative force in the evolution of this gene family. A comparative analysis of evolutionary rates at fifteen loci involved in innate, intrinsic and adaptive immunity, and mating systems revealed that more promiscuous species are on average under stronger selection at defense genes (Appendix C). Although the effect is weak, this suggests that sexual promiscuity plays some role in the evolution of immune loci by affecting the risk of contracting infectious diseases.
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Leung, Kit-Yi. "Molecular recognition between colicins and their immunity proteins." Thesis, University of East Anglia, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338294.

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Tusco, Radu. "Molecular mechanisms of selective autophagy in innate immunity." Thesis, University of Warwick, 2017. http://wrap.warwick.ac.uk/95261/.

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Autophagy is an evolutionarily conserved process of cellular material degradation, involved in development, starvation-induced nutrient-level control, degradation of aggregated proteins and pathogen removal. The specificity of this process is governed by selective autophagy receptors, messenger proteins which identify cargo and deliver it to Atg8a – a component of the core autophagic machinery. Receptors bind to Atg8-family proteins via the LIR motif, a short amino-acid sequence that is conserved across the animal kingdom. We performed a bioinformatics screen in order to identify new putative Atg8a interacting proteins. We searched the Drosophila proteome for proteins containing LIRmotifs and ubiquitin-binding domains. We identified the protein Kenny (homologue of human IKKg), which contains a LIR motif and a conserved UBAN domain. Kenny is a modulator of the Drosophila Immune deficiency (IMD) pathway, an innate immunity response targeted at gram-negative bacteria. Using biochemical approaches and in vivo studies in Drosophila we observed that Kenny interacted directly with Atg8a via its LIR motif and was selectively degraded by autophagy. We found that Kenny accumulated in autophagy depleted flies, which was accompanied by a constitutive activation of the IMD pathway and expression of antimicrobial peptides. This caused a hyperproliferation of stem cells in the midgut, reduced defecation rates and shortened the overall fly lifespan. Given sequence similarities between Kenny and another described receptor, Optineurin, we also investigated Kenny’s potential role in mitophagy and/or xenophagy. Kenny accumulated and localised with mitochondria in thorax muscles of flies, treated with FCCP. Kenny was found to localise in the vicinity of phagocytosed Staphylococcus aureus in larval haemocytes, cultured ex vivo. We propose that Optineurin could be a new functional mammalian orthologue of Kenny, in addition to the established mammalian homologue, NEMO.
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Watson, Aleksandra. "Molecular structure and function of C-type lectin-like molecules in innate immunity." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504625.

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Fytrou, Anastasia. "Drosophila immunity : QTL mapping, genetic variation and molecular evolution." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4742.

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Drosophila is involved in a wide range of interactions with parasites and pathogens (parasitoid wasps, bacteria, fungi, viruses). Drosophila hosts vary greatly at the species, population and individual level, in their response against such organisms, and much of this variation has a genetic basis. In this thesis I explored three aspects of this variation. First, using recombination mapping based on SNPs and a variation of bulk segregant analysis, I identified a QTL region on the right arm of the third chromosome of D. melanogaster associated with resistance to at least some of the parasitoid species / strains used in the experiments. The location of the QTL was further explored with deficiency complementation mapping and was narrowed down to the 96D1-97B1 region. The success of the deficiency mapping suggests that the resistant allele is not completely dominant. Second, I investigated patterns of molecular evolution in a set of immunity-related genes, using sequences from a D. melanogaster and a D. simulans population and a set of genes without known involvement in immunity for comparison. I found evidence that several of these genes have evolved under different selection pressure in each species, possibly indicating interactions with different parasites. The immunity genes tested appear to be evolving faster compared to non-immunity genes, supporting the idea that the immune system is evolving under strong selective pressure from parasites. Finally, in a D. melanogaster – sigma virus system, I measured genetic variation in the transmission of different virus genotypes, in different environments. There was poor correlation between temperatures, suggesting that environmental heterogeneity could constraint evolution of resistance (to virus transmission). The correlation between viral genotypes was also low, although relatively stronger for more closely phylogenetically related viral strains. Such interactions between host genotypes, virus genotypes and environmental conditions can maintain genetic variation in virus transmission.
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Kneeshaw, Sophie. "Molecular mechanisms of redoxin-mediated signalling in plant immunity." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/18754.

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Posttranslational modification (PTM) of proteins is essential to creating a diverse proteome with the complex functions necessary to regulate key cellular processes. Redox-based PTMs exhibit many desirable characteristics to finely modulate transcriptional regulators; they occur rapidly and can alter protein conformation, localisation and activity. The plant immune system offers an excellent model in which to study redox-based modifications due to the rapid accumulation of oxidising agents that occurs during immune invasion. This so-called “oxidative burst” causes spontaneous oxidation of cysteine residues that are present in many regulatory proteins. These modifications fine-tune the activities of proteins that harbour them, enabling them to act in a concerted effort to reprogram the transcriptome, prioritising the expression of immune-related genes over housekeeping genes. Disulphide bonds (S-S) and S-nitrosothiols (SNO, i.e. the addition of an NO group to a cysteine moiety) have been shown to play particularly important roles in plant immunity. However, what still remains unclear is how these redox-based PTMs are rendered reversible, enabling them to act as molecular signalling switches. The work presented in this thesis explores a class of enzymes that are responsible for controlling the cellular levels of protein oxidation: the Thioredoxins. In addition to their well-established role in reducing disulphide bonds, I demonstrate in Chapter 3 that Thioredoxins are able to reverse protein S-nitrosylation during plant immune signalling. Immune-inducible Thioredoxin-h5 (TRXh5) was shown to be unable to restore immunity in gsnor1 mutants that display excessive accumulation of the NO donor S-nitrosoglutathione, but rescued impaired immunity and defence gene expression in nox1-mutants that exhibit elevated levels of free NO. This data indicates that TRXh5 discriminates between protein-SNO substrates to provide previously unrecognized specificity and reversibility to protein-SNO signalling in plant immunity. Furthermore, data is presented to show that TRXh5 reversed the effects of S.nitrosylation on many immune-related transcriptional regulators in vitro, forming the initial stages of an investigation into which proteins and pathways might be controlled by reversible S-nitrosylation in plant immunity (Chapters 3 & 4). Although the majority of transcriptional regulators are likely modified at their site of action, the nucleus, very little is currently known about nuclear redox signalling in plants. Therefore, in Chapter 5 a subclass of theThioredoxin superfamily was studied, the Nucleoredoxins, which have previously been shown to display disulphide reduction activity and localise in part to the nucleus. Here it is revealed that the activity and nuclear accumulation of Nucleoredoxin 1 (NRX1) is induced by the plant leaf pathogen Pseudomonas syringae, suggesting a key role for this protein in immune signalling. Target-capture experiments and subsequent mass spectrometry analysis identified the first in vitro targets of NRX1 and revealed many proteins with roles in oxidative stress, including the hydrogen peroxide scavenger Catalase 2 (CAT2). Moreover, overexpression of NRX1 was shown to be able to rescue the enhanced cell death phenotype of cat2 knockout mutants in response to the oxidative stressor, methyl viologen. Accordingly, nrx1 knockout mutants also exhibited an enhanced cell death phenotype in response to methyl viologen treatment. Together, these data indicate that NRX1 plays a key role in the control of oxidative stress-mediated cell death, potentially through direct regulation of Catalase proteins. Taken together, the work in this thesis implicates members of the Thioredoxin family as key regulators of transcriptional reprogramming during plant immunity and uncovers a novel role for Thioredoxin superfamily member, NRX1, in the control of oxidative stress.
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Ma, Yan. "Molecular mechanisms of NLR pair-mediated immunity in Arabidopsis." Thesis, University of East Anglia, 2016. https://ueaeprints.uea.ac.uk/63111/.

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Central to plant survival is the ability to activate immunity upon pathogen perception. Plants deploy immune receptors to recognise specific pathogenderived molecules (effectors) and to trigger defence. These receptors usually recognise a specific effector, but some work in pairs and can detect multiple effectors. The Arabidopsis RRS1-R/RPS4 receptor pair forms an immune complex, conferring recognition of two distinct bacterial effectors, AvrRps4 and PopP2. A paralogous pair linked to RRS1/RPS4, designated as RRS1B/RPS4B, only recognises AvrRps4. My work has revealed that both pairs detect AvrRps4 via an integrated WRKY domain of RRS1 or RRS1B, which mimics the effector’s host targets: the WRKY transcription factors (TF). It has also been shown that the WRKY TF-targeting PopP2 is also perceived by the RRS1-R WRKY domain. Together, we suggest that RRS1 (or RRS1B) with the WRKY domain fusion has evolved to protect defence-regulating WRKY proteins from being attacked by effectors. These integrated domains of immune receptors are becoming popular targets for synthetic resistance engineering. However, one of the biggest challenges is to avoid auto-activity while enabling new recognition capacity when manipulating the integrated domains. To better understand how these receptors operate to convert effector perception into defence activation, I investigated the dynamic molecular interactions in the pre-activation complex, and those that change upon effector perception. I found that RRS1-R/RPS4 complex is negatively regulated by the WRKY domain during pre-activation, and effector-triggered activation is likely mediated by de-repression of the WRKY domain. After effector-triggered RRS1 de-repression, the activation signal is transduced to RPS4. Domain swaps between RRS1-R/RPS4 and RRS1B/RPS4B have revealed the key interaction required for this transduction is between RRS1 domain 4 and the RPS4 C-terminal domain. Furthermore, I discovered possible distinct domain-domain interactions that enable AvrRps4- and PopP2- triggered activation. The mechanistic insights into complex auto-inhibition and activation described in this thesis will prove valuable for many other cooperative immune receptor systems.
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Jun, Janice. "THE OFFENSE-DEFENSE BALANCE IN IMMUNITY." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1467997330.

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Books on the topic "Molecular immunity"

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Sessa, Guido. Molecular plant immunity. Chichester, West Sussex: Wiley-Blackwell, 2013.

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Sessa, Guido, ed. Molecular Plant Immunity. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481431.

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H, Lichtman Andrew, and Pillai Shiv, eds. Cellular and molecular immunology. 6th ed. Philadelphia: Saunders/Elsevier, 2010.

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H, Lichtman Andrew, ed. Cellular and molecular immunology. 5th ed. Philadelphia, PA: Saunders, 2005.

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H, Lichtman Andrew, and Pillai Shiv, eds. Cellular and molecular immunology. 6th ed. Philadelphia: Saunders Elsevier, 2007.

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H, Lichtman Andrew, and Pober Jordon S, eds. Cellular and molecular immunology. 2nd ed. Philadelphia: W.B. Saunders, 1994.

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H, Lichtman Andrew, and Pober Jordan S, eds. Cellular and molecular immunology. 3rd ed. Philadelphia: Saunders, 1997.

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H, Lichtman Andrew, and Pober Jordan S, eds. Cellular and molecular immunology. Philadelphia: Saunders, 1991.

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J, Wood Kathryn, ed. Principles of cellular and molecular immunology. Oxford: Oxford University Press, 1993.

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Reid, Kenneth B. M., and Robert B. Sim, eds. Molecular Aspects of Innate and Adaptive Immunity. Cambridge: Royal Society of Chemistry, 2008. http://dx.doi.org/10.1039/9781847558848.

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Book chapters on the topic "Molecular immunity"

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Foreman, Deborah B., and Suzanne Bohlson. "Innate Immunity." In Molecular Life Sciences, 1–14. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_120-2.

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Foreman, Deborah B., and Suzanne Bohlson. "Innate Immunity." In Molecular Life Sciences, 580–90. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_120.

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Giese, Matthias. "Mucosal Immunity." In Introduction to Molecular Vaccinology, 63–95. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25832-4_3.

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Carlberg, Carsten, and Eunike Velleuer. "Innate Immunity and Inflammation." In Molecular Immunology, 19–40. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04025-2_2.

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Park, Chang Jin, and Pamela C. Ronald. "The Rice Xa21 Immune Receptor Recognizes a Novel Bacterial Quorum Sensing Factor." In Molecular Plant Immunity, 1–21. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481431.ch1.

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Ökmen, Bilal, and Pierre J. G. M. de Wit. "Cladosporium fulvum-Tomato Pathosystem: Fungal Infection Strategy and Plant Responses." In Molecular Plant Immunity, 211–24. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481431.ch10.

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Westwood, Jack H., and John P. Carr. "Cucumber Mosaic Virus-ArabidopsisInteraction: Interplay of Virulence Strategies and Plant Responses." In Molecular Plant Immunity, 225–50. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481431.ch11.

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Chen, Yan-Jun, Michael F. Lyngkjaer, and David B. Collinge. "Future Prospects for Genetically Engineering Disease-Resistant Plants." In Molecular Plant Immunity, 251–75. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481431.ch12.

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Ma, Lisong, Harrold A. van den Burg, Ben J. C. Cornelissen, and Frank L. W. Takken. "Molecular Basis of Effector Recognition by Plant NB-LRR Proteins." In Molecular Plant Immunity, 23–40. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481431.ch2.

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Coaker, Gitta, and Douglas Baker. "Signal Transduction Pathways Activated by R Proteins." In Molecular Plant Immunity, 41–53. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481431.ch3.

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Conference papers on the topic "Molecular immunity"

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Chekanova, T. A., V. G. Akimkin, A. V. Kalenskaya, T. V. Tyrgina, and E. V. Tivanova. "FORMATION OF POPULATION IMMUNITY TO SARS-CoV-2 IN THE MOSCOW REGION." In Molecular Diagnostics and Biosafety. Federal Budget Institute of Science 'Central Research Institute for Epidemiology', 2020. http://dx.doi.org/10.36233/978-5-9900432-9-9-180.

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49 813 sera from persons without clinical symptoms of infectious diseases were tested for IgG to the nucleocapsid protein of SARS-CoV-2 at the Center for Molecular Diagnostics (Central Research Institute of Epidemiology) from May 22 to August 28, 2020. The dynamics of the incidence of seropositive persons was assessed by decades. The maximum seroprevalence was noted at the end of May. Seroprevalence indicators changed slightly from June 21 to August 28 (maximum values, about 17%, were noted from July 1 to July 20), which was consistent with the slowdown in the number of new cases of COVID-19 in the Moscow region.
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Ponomarenko, Julia, Kerrie Vaughan, Sinu Paul, Bjoern Peters, Alessandro Sette, Maximilian Haeussler, and Sebastian Maurer-Stroh. "Ebola: an analysis of immunity at the molecular level." In 2015 International Workshop on Artificial Immune Systems (AIS). IEEE, 2015. http://dx.doi.org/10.1109/aisw.2015.7469230.

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Collins, Natalie B., Robert Manguso, Hans Pope, and W. Nicholas Haining. "Abstract A16: Defining molecular mechanisms of resistance to tumor immunity." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-a16.

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Dranoff, Glenn. "Abstract PL07-03: Mechanisms of protective tumor immunity." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-pl07-03.

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Vries, Jolanda De, Winald Gerritsen, and Carl G. Figdor. "Abstract ED01-01: Immunity against cancer: How to be enhanced?" In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-ed01-01.

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Wang, Cindy, Carolyn Cao, Lisa Berman-Booty, Jesse Swanson, Rukiye Eraslan, Miguel Sanjuan, Gregory Vite, et al. "Abstract B198: Targeting CSK kinase activity to enhance antitumor immunity." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b198.

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Zhang, Zhibin, Ying Zhang, Shiyu Xia, Qing Kong, Shunying Li, Xing Liu, Caroline Junqueira, et al. "Abstract A022: Gasdermin E suppresses tumor growth by activating antitumor immunity." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-a022.

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Juric, Vladi, Chris Chan, Erin Mayes, Manith Norng, Tiep Le, Subhadra Dash, Venkataraman Sriram, et al. "Abstract C105: Targeting of TREM1+myeloid cells to promote antitumor immunity." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-c105.

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Li, Yu, Mingyang Song, Reiko Nishihara, Zhi Rong Qian, Raphaelle Varraso, Kentaro Inamura, Yohei Masugi, et al. "Abstract B11: Asthma and risk of colorectal cancer according to tumor immunity and molecular subtypes." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-b11.

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Angelidis, Ilias, Dimitrios Konstandopoulos, Dimitra Kerdidani, Emmanouil Aerakis, Katerina Douka, Dorothea Maneta, Ioannis Vamvakaris, et al. "Lung Cancer-Associated Fibroblasts in MHCII immunity: Understanding its Molecular Basis to Design Novel Immunotherapies." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.44.

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Reports on the topic "Molecular immunity"

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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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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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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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Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

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The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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Sessa, Guido, and Gregory B. Martin. molecular link from PAMP perception to a MAPK cascade associated with tomato disease resistance. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597918.bard.

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The research problem: The detection of pathogen-associated molecular patterns (PAMPs) by plant pattern recognition receptors (PRRs) is a key mechanism by which plants activate an effective immune response against pathogen attack. MAPK cascades are important signaling components downstream of PRRs that transduce the PAMP signal to activate various defense responses. Preliminary experiments suggested that the receptor-like cytoplasmickinase (RLCK) Mai5 plays a positive role in pattern-triggered immunity (PTI) and interacts with the MAPKKK M3Kε. We thus hypothesized that Mai5, as other RLCKs, functions as a component PRR complexes and acts as a molecular link between PAMP perception and activation of MAPK cascades. Original goals: The central goal of this research was to investigate the molecular mechanisms by which Mai5 and M3Kε regulate plant immunity. Specific objectives were to: 1. Determine the spectrum of PAMPs whose perception is transmitted by M3Kε; 2. Identify plant proteins that act downstream of M3Kε to mediate PTI; 3. Investigate how and where Mai5 interacts with M3Kε in the plant cell; 4. Examine the mechanism by which Mai5 contributes to PTI. Changes in research directions: We did not find convincing evidence for the involvement of M3Kε in PTI signaling and substituted objectives 1 and 3 with research activities aimed at the analysis of transcriptomic profiles of tomato plants during the onset of plant immunity, isolation of the novel tomato PRR FLS3, and investigation of the involvement of the RLCKBSKs in PTI. Main achievements during this research program are in the following major areas: 1. Functional characterization of Mai5. The function of Mai5 in PTI signaling was demonstrated by testing the effect of silencing the Mai5 gene by virus-induced gene silencing (VIGS) experiments and in cell death assays. Domains of Mai5 that interact with MAPKKKs and subcellular localization of Mai5 were analyzed in detail. 2. Analysis of transcriptional profiles during the tomato immune responses to Pseudomonas syringae (Pombo et al., 2014). We identified tomato genes whose expression is induced specifically in PTI or in effector-triggered immunity (ETI). Thirty ETI-specific genes were examined by VIGS for their involvement in immunity and the MAPKKK EPK1, was found to be required for ETI. 3. Dissection of MAP kinase cascades downstream of M3Kε (Oh et al., 2013; Teper et al., 2015). We identified genes that encode positive (SGT and EDS1) and negative (WRKY1 and WRKY2) regulators of the ETI-associated cell death mediated by M3Kε. In addition, the MKK2 MAPKK, which acts downstream of M3Kε, was found to interact with the MPK3 MAPK and specific MPK3 amino acids involved interaction were identified and found to be required for induction of cell death. We also identified 5 type III effectors of the bacterial pathogen Xanthomonaseuvesicatoria that inhibited cell death induced by components of ETI-associated MAP kinase cascades. 4. Isolation of the tomato PRR FLS3 (Hind et al., submitted). FLS3, a novel PRR of the LRR-RLK family that specifically recognizes the flagellinepitope flgII-28 was isolated. FLS3 was shown to bind flgII-28, to require kinase activity for function, to act in concert with BAK1, and to enhance disease resistance to Pseudomonas syringae. 5. Functional analysis of RLCKs of the brassinosteroid signaling kinase (BSK) family.Arabidopsis and tomato BSKs were found to interact with PRRs. In addition, certain ArabidospsisBSK mutants were found to be impaired in PAMP-induced resistance to Pseudomonas syringae. Scientific and agricultural significance: Our research activities discovered and characterized new molecular components of signaling pathways mediating recognition of invading pathogens and activation of immune responses against them. 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.
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Sessa, Guido, and Gregory Martin. MAP kinase cascades activated by SlMAPKKKε and their involvement in tomato resistance to bacterial pathogens. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7699834.bard.

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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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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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Gafni, Yedidya, and Vitaly Citovsky. Inactivation of SGS3 as Molecular Basis for RNA Silencing Suppression by TYLCV V2. United States Department of Agriculture, November 2013. http://dx.doi.org/10.32747/2013.7593402.bard.

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The Israeli isolate of Tomato yellow leaf curl geminivirus(TYLCV-Is) is a major tomato pathogen, causing extensive crop losses in Israel and in the south-eastern U.S. Yet, little is known about the molecular mechanisms of its interaction with tomato cells. One of the most interesting aspects of such interaction is how the invading virus counteracts the RNA silencing response of the plant. In the former BARD project, we have shown that TYLCV-Is V2 protein is an RNA silencing suppressor, and that this suppression is carried out via the interaction of V2 with the SGS3 component of the plant RNA silencing machinery. This reported project was meant to use our data as a foundation to elucidate the molecular mechanism by which V2 affects the SGS3 activity. While this research is likely to have an important impact on our understanding of basic biology of virus-plant interactions and suppression of plant immunity, it also will have practical implications, helping to conceive novel strategies for crop resistance to TYLCV-Is. Our preliminary data in regard to V2 activities and our present knowledge of the SGS3 function suggest likely mechanisms for the inhibitory effect of V2 on SGS3. We have shown that V2 possess structural and functional hallmarks of an F-box protein, suggesting that it may target SGS3 for proteasomal degradation. SGS3 contains an RNA-binding domain and likely functions to protect the cleavage produces of the primary transcript for subsequent conversion to double-stranded forms; thus, V2 may simply block the RNA binding activity of SGS3. V2 may also employ a combination of these mechanisms. These and other possibilities were tested in this reported project.
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Barefoot, Susan, Benjamin Juven, Thomas Hughes, Avraham Lalazar, A. B. Bodine, Yitzhak Ittah, and Bonita Glatz. Characterization of Bacteriocins Produced by Food Bioprocessing Propionobacteria. United States Department of Agriculture, August 1992. http://dx.doi.org/10.32747/1992.7561061.bard.

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Objectives were to further characterize activity spectra of dairy propionibacteria bacteriocins, jenseniin G and propionicin PLG-1, purify them, examine the role of cell walls in resistance, examine their interactions with cytoplasmic membrane, explain producer immunity, and clone the responsible genes. Inhibitory spectra of both bacteriocins were further characterized. Propionicin was most effective in controlling Gram-positive, rather than Gram-negative organisms; it controlled growth of sensitive cells both in a culture medium and a model food system. Jenseniin inhibited yogurt cultures and may help prevent yogurt over-acidification. Both were active against botulinal spores; jenseniin was sporostatic; propionicin was sporicidal. Jenseniin was produced in broth culture, was stable to pH and temperature extremes, and was purified. Its molecular mass (3649 Da) and partial amino acid composition (74%) were determined. A blocked jenseniin N-terminus prevented sequencing. Methods to produce propionicin in liquid culture were improved, and large scale culture protocols to yield high titers were developed. Methods to detect and quantify propionicin activity were optimized and standardized. Stability of partially purified propionicin was demonstrated and an improved purification scheme was developed. Purified propionicin had a 9328-Da molecular mass, contained 99 amino acids, and was significantly hydrophobic; ten N-terminal amino acids were identified. Propionicin and Jenseniin interacted with cytoplasmic membranes; resistance of insensitive species was cell wall-related. Propionicin and jenseniin acted similarly; their mode of action appeared to differ from nisin. Spontaneous jenseniin-resistant mutants were resistant to propionicin but nisin-sensitive. The basis for producer immunity was not resolved. Although bacteriocin genes were not cloned, a jenseniin producer DNA clone bank and three possible vectors for cloning genes in propionibacteria were constructed. In addition, transposon Tn916 was conjugatively transferred to the propionicin producer from chromosomal and plasmid locations at transfer frequencies high enough to permit use of Tn916 for insertional mutagenesis or targeting genes in propionibacteria. The results provide information about the bacteriocins that further supports their usefulness as adjuncts to increase food safety and/or quality.
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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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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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DeMartini, James C., Abraham Yaniv, Jonathan O. Carlson, Arnona Gazit, Leonard E. Pearson, Kalman Perk, J. K. Young, Noam Safran, and A. Friedman. Evaluation of Naked Proviral DNA as a Vaccine for Ovine Lentivirus Infection. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7570553.bard.

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Ovine lentivirus (OvLV) infection is widespread in sheep of the United States and Israel and is responsible for substantial economic losses. The primary goal of this project was to evaluate naked proviral DNA as a vaccine to induce protective immunity in sheep in endemic areas. Contrary to expectations, inoculation of sheep with proviral DNA derived from the full length OvLV molecular clone pkv72 did not result in detectable OvLV infection, but infectious virus was recovered from transfected ovine cells. Kv72 virus produced by these cells infected sheep and induced antibody responses, and was used as a viral challenge in subsequent experiments. To improve in vivo transfection efficiency and compare the viral LTR with other romoters, expression of reporter genes was studied in sheep transfected in vivo by injection of cationic liposome-DNA complexes; one formulation produced gene expression in a sheep for 4 months following a single intravenous injection. Since the pol-deleted OvLV construct was not stable in vivo, twelve lambs were injected with plasmids containing the Kv72 gag region (pCMVgag) or env region (pCMVenv), or saline. Prior to challenge, no detectable anti-OvLV immune responses were detected. Following homologous challenge with OvLV. Although the naked DNA approach to vaccination holds promise for control of ovine lentivirus-induced disease, further work needs to be done to develop more effective methods of transfecting sheep with DNA.
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