Gotowe bibliografie tematyczne / Immune response – Regulation

Gotowa bibliografia na temat „Immune response – Regulation”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 września 2023

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Artykuły w czasopismach na temat "Immune response – Regulation"

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Hurtley, S. M. "Immune Response Regulation". Science's STKE 2006, nr 358 (17.10.2006): tw366. http://dx.doi.org/10.1126/stke.3582006tw366.

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Sekenova, A., i V. Ogay. "Role of mesenchymal stem cells in the regulation of immune response". BULLETIN of the L.N. Gumilyov Eurasian National University. BIOSCIENCE Series 123, nr 2 (2018): 69–83. http://dx.doi.org/10.32523/2616-7034-2018-123-2-69-83.

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Cooke, A. "Regulation of the Immune Response". Diabetic Medicine 6, nr 1 (2.01.1989): 71–77. http://dx.doi.org/10.1111/j.1464-5491.1989.tb01143.x.

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Greene, Mark I., i Herman Waldmann. "Regulation of the immune response". Current Opinion in Immunology 22, nr 5 (październik 2010): 549–51. http://dx.doi.org/10.1016/j.coi.2010.09.004.

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Kelsoe, Garnett. "Regulation of the immune response". Cellular Immunology 98, nr 1 (marzec 1986): 145–55. http://dx.doi.org/10.1016/0008-8749(86)90275-3.

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Gazzinelli-Guimaraes, Pedro H., i Thomas B. Nutman. "Helminth parasites and immune regulation". F1000Research 7 (23.10.2018): 1685. http://dx.doi.org/10.12688/f1000research.15596.1.

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Helminth parasites are complex metazoans that belong to different taxonomic families but that collectively share the capacity to downregulate the host immune response directed toward themselves (parasite-specific immunoregulation). During long-standing chronic infection, these helminths appear able to suppress immune responses to bystander pathogens/antigens and atopic, autoimmune, and metabolic disorders. Helminth-induced immunoregulation occurs through the induction of regulatory T cells or Th2-type cells (or both). However, secreted or excreted parasite metabolites, proteins, or extracellular vesicles (or a combination of these) may also directly induce signaling pathways in host cells. Therefore, the focus of this review will be to highlight recent advances in understanding the immune responses to helminth infection, emphasizing the strategies/molecules and some of the mechanisms used by helminth parasites to modulate the immune response of their hosts.
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Bickett, Thomas E., i Sana D. Karam. "Tuberculosis–Cancer Parallels in Immune Response Regulation". International Journal of Molecular Sciences 21, nr 17 (26.08.2020): 6136. http://dx.doi.org/10.3390/ijms21176136.

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Mycobacterium tuberculosis and cancer are two diseases with proclivity for the development of resistance to the host immune system. Mechanisms behind resistance can be host derived or disease mediated, but they usually depend on the balance of pro-inflammatory to anti-inflammatory immune signals. Immunotherapies have been the focus of efforts to shift that balance and drive the response required for diseases eradication. The immune response to tuberculosis has widely been thought to be T cell dependent, with the majority of research focused on T cell responses. However, the past decade has seen greater recognition of the importance of the innate immune response, highlighting factors such as trained innate immunity and macrophage polarization to mycobacterial clearance. At the same time, there has been a renaissance of immunotherapy treatments for cancer since the first checkpoint inhibitor passed clinical trials, in addition to work highlighting the importance of innate immune responses to cancer. However, there is still much to learn about host-derived responses and the development of resistance to new cancer therapies. This review examines the similarities between the immune responses to cancer and tuberculosis with the hope that their commonalities will facilitate research collaboration and discovery.
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Ernst, P. B., V. E. Reyes, S. E. Crowe, H. Haeberle, G. Ye, F. Song, K. B. Bamford i G. R. Klimpel. "Regulation of the mucosal immune response." American Journal of Tropical Medicine and Hygiene 60, nr 4_suppl (1.04.1999): 2–9. http://dx.doi.org/10.4269/ajtmh.1999.60.2.

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Lipniacki, Tomasz, Pawel Paszek, Allan R. Brasier, Bruce A. Luxon i Marek Kimmel. "Stochastic Regulation in Early Immune Response". Biophysical Journal 90, nr 3 (luty 2006): 725–42. http://dx.doi.org/10.1529/biophysj.104.056754.

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Siskind, Gregory W., i Eduardo Arreaza. "Network Regulation of the Immune Response". Allergy and Asthma Proceedings 10, nr 6 (1.11.1989): 387–91. http://dx.doi.org/10.2500/108854189778935872.

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Rozprawy doktorskie na temat "Immune response – Regulation"

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Dahal, Lekh Nath. "Soluble CTLA-4 and immune regulation". Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=202565.

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Madera, Laurence. "Mechanisms of immune response regulation by innate defense regulator peptides". Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43066.

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The growing threat of antibiotic-resistant bacteria necessitates the development of new anti-infective therapeutics. Innate defense regulator (IDR) peptides are a novel class of immunomodulatory agents shown to combat bacterial pathogens in murine models of infection via the augmentation of host immune functions, including the stimulation of chemokine production and enhancement of leukocyte recruitment, while suppressing bacterial-induced inflammation. Although IDR-peptides present the potential for future broad-range anti-infective agents, our limited understanding of how they modulate host immunity remains an obstacle in their development as clinical therapeutics. I hypothesized that IDR-peptides impact host immunity by modulating the immune responses of monocytes, a cell population necessary for IDR-mediated protection against infection. In this study, IDR-1002 was found to be a multi-faceted regulator of monocyte migration. IDR-1002 induced the production of monocyte-specific chemokines MCP-1 and MCP-3, as well as neutrophil-specific chemokines, IL-8 and GRO-α in human peripheral blood mononuclear cells (PBMCs), correlating with the activation of the mitogen-activated protein kinases (MAPK), p38 and extracellular-regulated kinase (ERK)-1/2, in monocytes. IDR-1002 was also found to enhance human monocyte migration towards chemokines through the enhancement of β1-integrin-mediated adhesion to fibronectin via regulation of the phosphatidylinositol-3-kinase (PI3K)-Akt signalling pathway. In addition, IDR-1002 increased monocyte responsiveness to the chemokines MIP-1α and RANTES via modulation of CCR5 expression. These results demonstrate an overall promotion of monocyte motility by IDR-1002. In contrast to the immune-strengthening effects of IDR-1002, the production of pro-inflammatory cytokines in human PBMCs stimulated with bacterial lipopolysaccharide (LPS) was suppressed by the peptide, and correlated with a suppression of LPS-induced NFκB and p38 MAPK signalling and activation of PI3K-Akt signalling in monocytes. These results demonstrate that IDR-peptides are potent modulators of human monocyte function via their extensive regulation of monocyte signalling networks, potentially accounting for their multifunctional effects on host immunity in murine models of bacterial infection.
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Cheung, Ka-wa Benny. "Immune regulation in response to mycobacterial infection". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634206.

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Cheung, Ka-wa Benny, i 張嘉華. "Immune regulation in response to mycobacterial infection". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634206.

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Alasoo, Kaur. "Regulation of gene expression in macrophage immune response". Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/263855.

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Gene expression quantitative trait loci (eQTL) mapping studies can provide mechanistic insights into the functions of disease-associated variants. However, many eQTLs are cell type and context specific. This is particularly relevant for immune cells, whose cellular function and behaviour can be substantially altered by external cues. Furthermore, understanding mechanisms behind eQTLs is hindered by the difficulty of identifying causal variants. We differentiated macrophages from induced pluripotent stem cells from 86 unrelated, healthy individuals derived as part of the Human Induced Pluripotent Stem Cells Initiative. We generated RNA-seq data from these cells in four experimental conditions: naïve, interferon- gamma (IFNɣ) treatment (18h), Salmonella infection (5h), and IFNγ treatment followed by Salmonella infection. We also measured chromatin accessibility with ATAC-seq in 31-42 individuals in the same four conditions. We detected gene expression QTLs (eQTLs) for 4326 genes, over 900 of which were condition-specific. We also detected a similar number of transcript ratio QTLs (trQTLs) that influenced mRNA processing and alternative splicing. Macrophage eQTLs and trQTLs were enriched for variants associated with Alzheimer’s disease, multiple autoimmune disorders and lipid traits. We also detected chromatin accessibility QTLs (caQTLs) for 14,602 accessible regions, including hundreds of long-range interactions. Joint analysis of eQTLs with caQTLs allowed us to greatly reduce the set of credible causal variants, often pinpointing to a single most likely variant. We found that caQTLs were less condition- specific than eQTLs and ~50% of the stimulation-specific eQTLs manifested on the chromatin level already in the naive cells. These observations might help to explain the discrepancy between strong enrichment of diseases associations in regulatory elements but only modest overlap with current eQTL studies, suggesting that many regulatory elements are in a ‘primed’ state waiting for an appropriate environmental signal before regulating gene expression.
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Lim, Andrew Yih-Fan. "Mechanisms of immune regulation in HIV disease". University of Western Australia. School of Surgery and Pathology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0081.

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[Truncated abstract] HIV infection compromises the ability of the host to mount effective immune responses. In untreated HIV disease, immune activation drives high rates of cell turnover and apoptosis, ultimately leading to abnormal and dysregulated cellular function. Immune activation may also induce the expansion of CD4+ regulatory T (Treg) cell populations capable of suppressing anti-HIV responses. Treatment with antiretroviral therapy (ART) allows the recovery of CD4+ T cell numbers in most patients. Persistent deficiencies in the number and function of CD4+ T cells seen in a proportion of individuals may reflect elevated numbers of Treg cells or an imbalanced regulatory-to-effector cytokine milieu. Furthermore, some patients develop paradoxical illnesses associated with the recovery of cellular function, known as immune restoration disease (IRD). The first part of this thesis addresses the role of CD4+ Treg cells in untreated and treated HIV disease. The second part addresses the phenotype of immune cells that express IL-10 and its receptor in untreated and treated patients, and the role of IL-10 in mycobacterial IRD. Firstly, several cell surface markers were evaluated to find a flow cytometry assay that could be used routinely to identify CD4+ Treg cells in HIV-infected patients. I tested CD25, GITR, CTLA-4, NRP-1 and LAG-3, but their expression did not mirror the expression of FoxP3, an intracellular transcription factor specific to CD4+ Treg cells (Chapter 2). Two published studies then described the use of CD127 to identify CD4+FoxP3+ Treg cells in humans. Using CD127, I determined the proportions and numbers of CD4+ Treg cells in untreated HIV-infected patients and in patients in their first year of ART. Proportions of CD4+ Treg cells correlated with the proportions of activated (HLA-DRHI) CD4+ T cells and with plasma HIV RNA levels in untreated patients, but showed an inverse correlation with CD4+ T cell count. In both untreated and treated patients, the proportions and numbers of FoxP3+ cells that expressed CD8 were significantly higher than in uninfected donors. This was clearest in patients with CD4+ T cell counts below 300/'L (Chapter 3). This body of work suggests that the frequencies of CD4+ Treg cells are directly related to the level of HIV-associated immune activation. Phenotyping of FoxP3+CD4+ Treg cells in untreated and treated patients and in uninfected donors revealed that co-expression of CD45RO, CD28, CTLA-4 and markers of activation were similar in all HIV-infected patients and controls. ii FoxP3+CD8+ T cells exhibit lower levels of CD45RO, CD28 and CTLA-4, but higher expression of PD-1 and CD57 (Chapter 4). This suggests that FoxP3+CD8+ T cells may have a reduced functional capacity. It is unclear whether they have regulatory activity by virtue of FoxP3 expression. ... Both patients produced higher levels of IFN? compared with IL-10 in response to mycobacterial antigens. In contrast, patients who experienced uneventful immune reconstitution produced higher levels of IL-10 (Chapter 6). Part 1 of this thesis highlights the importance of using specific cellular markers to identify CD4+ Treg cells, and confirms CD127 as a valuable marker for routine monitoring of blood Treg cells. Part 2 of this thesis demonstrates the important regulatory role of IL-10 in patients receiving ART.
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Källberg, Eva. "Regulation of the immune response; focusing on somatic hyper-mutation". Lund : Lund University, Dept. of Cell and Molecular Biology, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39071819.html.

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Mehta, Ninad T. "Early Epigenetic Regulation of the Adaptive Immune Response Gene CIITA". Digital Archive @ GSU, 2010. http://digitalarchive.gsu.edu/biology_theses/24.

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The precise regulation of Major Histocompatibility class II (MHC-II) genes plays an important role in the control of the adaptive immune response. MHC-II genes are expressed constitutively in only a few cell types, but their expression can be induced by the inflammatory response cytokine interferon gamma (INF-γ). The regulation of MHC-II is controlled by a Master Regulator, the class II transactivator (CIITA). Multiple studies have shown that CIITA regulated expression of MHC-II is controlled and induced by INF-γ. It has been also shown that a functional CIITA gene is necessary for the expression of MHC-II genes. CIITA is thus a general regulator of both constitutive and inducible MHC-II expression. Although much is known about the transcription factors necessary for CIITA expression, there is little information as to the epigenetic modifications and the requisite enzymes needed to provide these transcription factors access to DNA. Previous studies in the Greer lab have shown that increased levels of acetylation of histones H3 upon INF-γ stimulation, as does tri-methylation of H3K4 upon prolonged cytokine stimulation. Similar observations were made at early time points post IFN-γ stimulation, where there is an instantaneous increase in the levels of H3K18ac and H3K4me3. In contrast to this, the levels of silencing modifications begin to drop with in the first 20 minutes of IFN-γ stimulation. The binding of STAT1 reaches its peak at about 60 minutes and the first transcripts for the protein start to appear as early as 40 minutes post the cytokines stimulation. Our study is the first to link the rapidly occurring epigenetic changes at the CIITA promoter pIV to EZH2
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Wheway, Julie Elizabeth School of Medicine UNSW. "The Y1 receptor for NPY: a novel regulator of immune cell function". Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/25194.

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Psychological conditions, including stress, compromise immune defenses. Although this concept is not novel, the molecular mechanism behind it remains unclear. Neuropeptide Y (NPY), regulates anxiety and is a part of the stress response. The NPY system also modulates immune functions such as cytokine release, cell migration, and innate immune cell activity. Postganglionic sympathetic nerves innervating lymphoid organs release NPY, which together with other peptides activate five receptors (Y1, Y2, Y4, Y5, and y6). Additionally, immune cells themselves release NPY following activation. Previous studies have shown that Y1 mediates NPY-immune effects and data presented here shows expression of Y1 on a wide range of immune cells. Results presented in this thesis, using Y1-deficient mice (Y1-/-), have uncovered a novel role for Y1 on immune cells. NPY acts endogenously to inhibit T cell activation whereas Y1-/- T cells are hyper-responsive to activation and trigger severe colitis after transfer into lymphopenic mice. Thus, signalling through the Y1 receptor on T cells inhibits T cell activation and controls the magnitude of T cell responses. Paradoxically, in Y1-/- mice, T cell differentiation to Th1 T cells appears to be defective as these mice were resistant to T helper type 1 (Th1) cell???mediated inflammatory responses and showed reduced levels of the Th1 cell???promoting cytokine interleukin 12 and reduced interferon ?? production. This defect was due to functionally impaired antigen presenting cells (APCs). Y1-deficient APCs are defective in their ability to produce Th1-promoting cytokines and present antigens to T cells and consequently, Y1-/- mice had reduced numbers of effector T cells. Key reciprocal bone marrow chimera experiments indicated that this effect is intrinsic to immune cells and not driven by other Y1-expressing cell types. These results demonstrate a fundamental bimodal role for the Y1 receptor in the immune system, serving as a strong negative regulator on T cells as well as a key activator of APC function. The findings presented in this thesis uncover a sophisticated molecular mechanism regulating immune cell functions and thus adds to a growing number of signalling pathways shared by the immune and nervous system.
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Cheung, Ka-wa Benny, i 張嘉華. "Mechanism of Bacillus Calmette Guerin-induced immune response". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29488989.

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Książki na temat "Immune response – Regulation"

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Marc, Feldmann, i Mitchison N. Avrion, red. Immune regulation. Clifton, N.J: Humana Press, 1985.

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Mediators of Immune Regulation and Immunotherapy (Conference) (1985 University of Western Ontario). Mediators of immune regulation and immunotherapy: Proceedings of the international symposium, Mediators of Immune Regulation and Immunotherapy, held June 13-15, 1985, at the University of Western Ontario, London, Ontario, Canada. Redaktorzy Singhal S. K i Delovitch T. L. New York: Elsevier, 1986.

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1956-, Srivastava Rakesh, Ram Bhanu P. 1951- i Tyle Praveen 1960-, red. Molecular mechanisms of immune regulation. New York, N.Y: VCH Publishers, 1991.

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S, Stolen Joanne, red. Modulators of immune responses: The evolutionary trail. Fair Haven, NJ: SOS Publications, 1996.

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1954-, Kresina Thomas F., red. Immune modulating agents. New York: M. Dekker, 1998.

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Bona, Constantin. Regulatory idiotopes. New York: Wiley, 1987.

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Nikolaevna, Alekseeva Irina, i Instytut fiziolohiï im. O.O. Bohomolʹt͡s︡i͡a︡., red. Pechenʹ i immunologicheskai͡a︡ reaktivnostʹ. Kiev: Nauk. dumka, 1991.

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International, Conference on Lymphocyte Activation and Immune Regulation (2nd 1988 Newport Beach Calif ). Mechanisms of lymphocyte activation and immune regulation II. New York: Plenum Press, 1989.

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Sudhir, Gupta, Paul William E i Fauci Anthony S. 1940-, red. Mechanisms of lymphocyte activation and immune regulation. New York: Plenum Press, 1987.

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Sudhir, Gupta, Paul William E i Fauci Anthony S, red. Mechanisms of lymphocyte activation and immune regulation. New York: Plenum Press, 1987.

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Części książek na temat "Immune response – Regulation"

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Katz, David R. "Inducer Accessory Cells as Regulators of the Immune Response". W Immune Regulation, 303–9. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4996-2_37.

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Belkaid, Yasmine, Sharvan Sehrawat i Barry T. Rouse. "Regulation of Antimicrobial Immunity". W The Immune Response to Infection, 109–20. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch8.

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Rotondo, Dino. "Prostaglandins and the Acute Phase Immune Response". W Temperature Regulation, 53–58. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-8491-4_9.

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Anderson, Ana C., i Vijay K. Kuchroo. "Autoimmune Response and Immune Tolerance". W Immune Regulation and Immunotherapy in Autoimmune Disease, 3–19. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-36003-4_1.

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Ksander, Bruce R., i Wayne Streilein. "Regulation of the Immune Response within Privileged Sites (Part 1 of 2)". W Mechanisms of Immune Regulation, 117–31. Basel: KARGER, 1994. http://dx.doi.org/10.1159/000319222.

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Ksander, Bruce R., i Wayne Streilein. "Regulation of the Immune Response within Privileged Sites (Part 2 of 2)". W Mechanisms of Immune Regulation, 132–45. Basel: KARGER, 1994. http://dx.doi.org/10.1159/000319223.

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Ayala, Alfred, Chun-Shiang Chung, Grace Y. Song, Patricia S. Grutkoski i H. Hank Simms. "Down-Regulation of the Immune Response". W Immunology and Infectious Disease, 41–78. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0245-6_3.

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Calder, Philip C., i Parveen Yaqoob. "Nutrient Regulation of the Immune Response". W Present Knowledge in Nutrition, 688–708. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781119946045.ch44.

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Kloubert, Veronika, i Lothar Rink. "Zinc Regulation of the Immune Response". W Nutrition, Immunity, and Infection, 245–78. Boca Raton : Taylor & Francis, 2018.: CRC Press, 2017. http://dx.doi.org/10.1201/9781315118901-15.

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Valdor, Rut. "Autophagy and Regulation of Immune Response". W Autophagy and Signaling, 93–118. Boca Raton, FL : CRC Press, 2018. | Series: Methods in signal transduction series: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120638-8.

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Streszczenia konferencji na temat "Immune response – Regulation"

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Verhoeven, Victoria I. "Immune response regulation inDermacentor variabilis". W 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.108512.

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Chigvintsev, Vladimir M., Petr V. Trusov i Natalya V. Zaitseva. "Mathematical model of antitumor immune response of organism regulation". W 29TH RUSSIAN CONFERENCE ON MATHEMATICAL MODELLING IN NATURAL SCIENCES. AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0059532.

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Morgan, Carrie I., Ping Zhou, John R. Ledford i Kristen Page. "Zinc Modulation Of The Innate Immune Response Via Regulation Of A20". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1064.

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El Sheikh, M., I. Angers i S. T. Qureshi. "Genetic Regulation of the Host Immune Response to Cryptococcus Neoformans Infection". W American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1211.

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Lyman, Cole A., Mark Clement, Travis J. A. Craddock, Mary Fletcher, Nancy G. Klimas i Gordon Broderick. "Feedback Regulation of Immune Response to Maximum Exercise in Gulf War Illness". W BCB '19: 10th ACM International Conference on Bioinformatics, Computational Biology and Health Informatics. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3307339.3342188.

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Schmit, Stephanie L., Ya-Yu Tsai, Joseph Bonner, Rebeca Sanz-Pamplona, Amit D. Joshi, Sidney S. Lindsey, Marilena Melas i in. "Abstract 824: Germline genetic regulation of the adaptive immune response in colorectal cancer". W Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-824.

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Osinska, Iwona, Anna Stelmaszczyk-Emmel, Malgorzata Polubiec-Kownacka, Dariusz Dziedzic i Joanna Domagala-Kulawik. "CTLA-4 on regulatory T cells - Regulation of local immune response in lung cancer". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa532.

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Redd, Priscilla S., Chunwan Lu, John D. Klement, Mohammed Ibrahim, Dafeng Yang, Daniela Payne, Iryna Lebedyeva i Kebin Liu. "Abstract 2263: Ceramide mimetics regulation of tumor cell response to immune checkpoint inhibitor immunotherapy". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2263.

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Redd, Priscilla S., Chunwan Lu, John D. Klement, Mohammed Ibrahim, Dafeng Yang, Daniela Payne, Iryna Lebedyeva i Kebin Liu. "Abstract 2263: Ceramide mimetics regulation of tumor cell response to immune checkpoint inhibitor immunotherapy". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2263.

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Sisler, Daniel, Sean Korpela, Natalia Gurule, Trista Hinz, Lindsay Marek, Bonnie Bullock, Howard Li i in. "Abstract B51: MAPK regulation of an innate immune response in KRAS-mutant lung adenocarcinoma". W Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-b51.

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Raporty organizacyjne na temat "Immune response – Regulation"

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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann i Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, luty 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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Splitter, Gary, Zeev Trainin i Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, lipiec 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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Nelson, Corwin D., Donald C. Beitz, Timothy A. Reinhardt i John D. Lippolis. Regulation of Immune Responses to Mycobacteria bovis by a Paracrine Mechanism of Vitamin D Signaling in Cattle. Ames (Iowa): Iowa State University, styczeń 2011. http://dx.doi.org/10.31274/ans_air-180814-646.

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Splitter, Gary A., Menachem Banai i Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, styczeń 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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Chejanovsky, Nor, Diana Cox-Foster, Victoria Soroker i Ron Ophir. Honeybee modulation of infection with the Israeli acute paralysis virus, in asymptomatic, acutely infected and CCD colonies. United States Department of Agriculture, grudzień 2013. http://dx.doi.org/10.32747/2013.7594392.bard.

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Honey bee (Apis mellifera) colony losses pose a severe risk to the food chain. The IAPV (Israeli acute paralysis virus) was correlated with CCD, a particular case of colony collapse. Honey bees severely infected with IAPV show shivering wings that progress to paralysis and subsequent death. Bee viruses, including IAPV, are widely present in honey bee colonies but often there are no pathological symptoms. Infestation of the beehive with Varroa mites or exposure to stress factors leads to significant increase in viral titers and fatal infections. We hypothesized that the honey bee is regulating/controlling IAPV and viral infections in asymptomatic infections and this control is broken through "stress" leading to acute infections and/or CCD. Our aims were: 1. To discover genetic changes in IAPV that may affect tissue tropism in the host, and/or virus infectivity and pathogenicity. 2. To elucidate mechanisms used by the host to regulate/ manage the IAPV-infection in vivo and in vitro. To achieve the above objectives we first studied stress-induced virus activation. Our data indicated that some pesticides, including myclobutanil, chlorothalonil and fluvalinate, result in amplified viral titers when bees are exposed at sub lethal levels by a single feeding. Analysis of the level of immune-related bee genes indicated that CCD-colonies exhibit altered and weaker immune responses than healthy colonies. Given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies were able to elicit this particular antiviral response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed high frequency of small interfering RNAs (siRNA) perfectly matching IAPV, Kashmir bee virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi pattern of targeting the viral genome .Our findings were further supported by analysis of samples from colonies experimentally infected with IAPV. Following for the first time the dynamics of IAPV infection in a group of CCD colonies that we rescued from collapse, we found that IAPV conserves its potential to act as one lethal, infectious factor and that its continuous replication in CCD colonies deeply affects their health and survival. Ours is the first report on the dominant role of IAPV in CCD-colonies outside from the US under natural conditions. We concluded that CCD-colonies do exhibit a regular siRNA response that is specific against predominant viruses associated with colony losses and other immune pathways may account for their weak immune response towards virus infection. Our findings: 1. Reveal that preventive measures should be taken by the beekeepers to avoid insecticide-based stress induction of viral infections as well as to manage CCD colonies as a source of highly infectious viruses such as IAPV. 2. Contribute to identify honey bee mechanisms involved in managing viral infections.
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Sessa, Guido, i Gregory Martin. role of FLS3 and BSK830 in pattern-triggered immunity in tomato. United States Department of Agriculture, styczeń 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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Avni, Adi, i Gitta L. Coaker. Proteomic investigation of a tomato receptor like protein recognizing fungal pathogens. United States Department of Agriculture, styczeń 2015. http://dx.doi.org/10.32747/2015.7600030.bard.

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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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Fluhr, Robert, i Maor Bar-Peled. Novel Lectin Controls Wound-responses in Arabidopsis. United States Department of Agriculture, styczeń 2012. http://dx.doi.org/10.32747/2012.7697123.bard.

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Innate immune responses in animals and plants involve receptors that recognize microbe-associated molecules. In plants, one set of this defense system is characterized by large families of TIR–nucleotide binding site–leucine-rich repeat (TIR-NBS-LRR) resistance genes. The direct interaction between plant proteins harboring the TIR domain with proteins that transmit and facilitate a signaling pathway has yet to be shown. The Arabidopsis genome encodes TIR-domain containing genes that lack NBS and LRR whose functions are unknown. Here we investigated the functional role of such protein, TLW1 (TIR LECTIN WOUNDRESPONSIVE1). The TLW1 gene encodes a protein with two domains: a TIR domain linked to a lectin-containing domain. Our specific aim in this proposal was to examine the ramifications of the TL1-glycan interaction by; A) The functional characterization of TL1 activity in the context of plant wound response and B) Examine the hypothesis that wounding induced specific polysaccharides and examine them as candidates for TL-1 interactive glycan compounds. The Weizmann group showed TLW1 transcripts are rapidly induced by wounding in a JA-independent pathway and T-DNA-tagged tlw1 mutants that lack TLW1 transcripts, fail to initiate the full systemic wound response. Transcriptome methodology analysis was set up and transcriptome analyses indicates a two-fold reduced level of JA-responsive but not JA-independent transcripts. The TIR domain of TLW1 was found to interact directly with the KAT2/PED1 gene product responsible for the final b-oxidation steps in peroxisomal-basedJA biosynthesis. To identify potential binding target(s) of TL1 in plant wound response, the CCRC group first expressed recombinant TL1 in bacterial cells and optimized conditions for the protein expression. TL1 was most highly expressed in ArcticExpress cell line. Different types of extraction buffers and extraction methods were used to prepare plant extracts for TL1 binding assay. Optimized condition for glycan labeling was determined, and 2-aminobenzamide was used to label plant extracts. Sensitivity of MALDI and LC-MS using standard glycans. THAP (2,4,6- Trihydroxyacetophenone) showed minimal background peaks at positive mode of MALDI, however, it was insensitive with a minimum detection level of 100 ng. Using LC-MS, sensitivity was highly increased enough to detect 30 pmol concentration. However, patterns of total glycans displayed no significant difference between different extraction conditions when samples were separated with Dionex ICS-2000 ion chromatography system. Transgenic plants over-expressing lectin domains were generated to obtain active lectin domain in plant cells. Insertion of the overexpression construct into the plant genome was confirmed by antibiotic selection and genomic DNA PCR. However, RT-PCR analysis was not able to detect increased level of the transcripts. Binding ability of azelaic acid to recombinant TL1. Azelaic acid was detected in GST-TL1 elution fraction, however, DHB matrix has the same mass in background signals, which needs to be further tested on other matrices. The major findings showed the importance of TLW1 in regulating wound response. The findings demonstrate completely novel and unexpected TIR domain interactions and reveal a control nexus and mechanism that contributes to the propagation of wound responses in Arabidopsis. The implications are to our understanding of the function of TIR domains and to the notion that early molecular events occur systemically within minutes of a plant sustaining a wound. A WEB site (http://genome.weizmann.ac.il/hormonometer/) was set up that enables scientists to interact with a collated plant hormone database.
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Meidan, Rina, i Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, styczeń 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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Brosh, Arieh, Gordon Carstens, Kristen Johnson, Ariel Shabtay, Joshuah Miron, Yoav Aharoni, Luis Tedeschi i Ilan Halachmi. Enhancing Sustainability of Cattle Production Systems through Discovery of Biomarkers for Feed Efficiency. United States Department of Agriculture, lipiec 2011. http://dx.doi.org/10.32747/2011.7592644.bard.

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Feed inputs represent the largest variable cost of producing meat and milk from ruminant animals. Thus, strategies that improve the efficiency of feed utilization are needed to improve the global competitiveness of Israeli and U.S. cattle industries, and mitigate their environmental impact through reductions in nutrient excretions and greenhouse gas emissions. Implementation of innovative technologies that will enhance genetic merit for feed efficiency is arguably one of the most cost-effective strategies to meet future demands for animal-protein foods in an environmentally sustainable manner. While considerable genetic variation in feed efficiency exist within cattle populations, the expense of measuring individual-animal feed intake has precluded implementation of selection programs that target this trait. Residual feed intake (RFI) is a trait that quantifies between-animal variation in feed intake beyond that expected to meet energy requirements for maintenance and production, with efficient animals being those that eat less than expected for a given size and level of production. There remains a critical need to understand the biological drivers for genetic variation in RFI to facilitate development of effective selection programs in the future. Therefore, the aim of this project was to determine the biological basis for phenotypic variation in RFI of growing and lactating cattle, and discover metabolic biomarkers of RFI for early and more cost-effective selection of cattle for feed efficiency. Objectives were to: (1) Characterize the phenotypic relationships between RFI and production traits (growth or lactation), (2) Quantify inter-animal variation in residual HP, (3) Determine if divergent RFIphenotypes differ in HP, residual HP, recovered energy and digestibility, and (4) Determine if divergent RFI phenotypes differ in physical activity, feeding behavior traits, serum hormones and metabolites and hepatic mitochondrial traits. The major research findings from this project to date include: In lactating dairy cattle, substantial phenotypic variation in RFI was demonstrated as cows classified as having low RMEI consumed 17% less MEI than high-RMEI cows despite having similar body size and lactation productivity. Further, between-animal variation in RMEI was found to moderately associated with differences in RHP demonstrating that maintenance energy requirements contribute to observed differences in RFI. Quantifying energetic efficiency of dairy cows using RHP revealed that substantial changes occur as week of lactation advances—thus it will be critical to measure RMEI at a standardized stage of lactation. Finally, to determine RMEI in lactating dairy cows, individual DMI and production data should be collected for a minimum of 6 wk. We demonstrated that a favorably association exists between RFI in growing heifers and efficiency of forage utilization in pregnant cows. Therefore, results indicate that female progeny from parents selected for low RFI during postweaning development will also be efficient as mature females, which has positive implications for both dairy and beef cattle industries. Results from the beef cattle studies further extend our knowledge regarding the biological drivers of phenotypic variation in RFI of growing animals, and demonstrate that significant differences in feeding behavioral patterns, digestibility and heart rate exist between animals with divergent RFI. Feeding behavior traits may be an effective biomarker trait for RFI in beef and dairy cattle. There are differences in mitochondrial acceptor control and respiratory control ratios between calves with divergent RFI suggesting that variation in mitochondrial metabolism may be visible at the genome level. Multiple genes associated with mitochondrial energy processes are altered by RFI phenotype and some of these genes are associated with mitochondrial energy expenditure and major cellular pathways involved in regulation of immune responses and energy metabolism.
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