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Relevant bibliographies by topics / Regulatory T cell

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Academic literature on the topic 'Regulatory T cell'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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Journal articles on the topic "Regulatory T cell"

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ZHOU, Zhou, Juan FENG, and Xian WANG. "Regulatory T Cell Differentiation and Regulators." ACTA BIOPHYSICA SINICA 28, no. 2 (2012): 93. http://dx.doi.org/10.3724/sp.j.1260.2012.20002.

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Ait-Oufella, Hafid, and Alain Tedgui. "Regulatory T-Cell Plasticity." Circulation Research 118, no. 10 (May 13, 2016): 1461–63. http://dx.doi.org/10.1161/circresaha.116.308805.

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Bashyam, Hema. "Regulatory T cell brakes." Journal of Experimental Medicine 205, no. 3 (February 18, 2008): 505. http://dx.doi.org/10.1084/jem.2053iti1.

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Savage, Peter A., David E. J. Klawon, and Christine H. Miller. "Regulatory T Cell Development." Annual Review of Immunology 38, no. 1 (April 26, 2020): 421–53. http://dx.doi.org/10.1146/annurev-immunol-100219-020937.

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Foxp3-expressing CD4+ regulatory T (Treg) cells play key roles in the prevention of autoimmunity and the maintenance of immune homeostasis and represent a major barrier to the induction of robust antitumor immune responses. Thus, a clear understanding of the mechanisms coordinating Treg cell differentiation is crucial for understanding numerous facets of health and disease and for developing approaches to modulate Treg cells for clinical benefit. Here, we discuss current knowledge of the signals that coordinate Treg cell development, the antigen-presenting cell types that direct Treg cell selection, and the nature of endogenous Treg cell ligands, focusing on evidence from studies in mice. We also highlight recent advances in this area and identify key unanswered questions.

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Rosenblum, Michael D., Sing Sing Way, and Abul K. Abbas. "Regulatory T cell memory." Nature Reviews Immunology 16, no. 2 (December 21, 2015): 90–101. http://dx.doi.org/10.1038/nri.2015.1.

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Ward-Hartstonge, Kirsten A., and Ajithkumar Vasanthakumar. "Regulatory T-cell heterogeneity." Clinical & Translational Immunology 7, no. 3 (2018): e01012. http://dx.doi.org/10.1002/cti2.1012.

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Scott, David W. "T regulatory cells turn on T regulatory cells." Blood 114, no. 19 (November 5, 2009): 3975–76. http://dx.doi.org/10.1182/blood-2009-09-241406.

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Yano, Hiroki, Takashi Ishida, Atsushi Inagaki, Toshihiko Ishii, Shigeru Kusumoto, Hirokazu Komatsu, Shinsuke Iida, Atae Utsunomiya, and Ryuzo Ueda. "Regulatory T-cell function of adult T-cell leukemia/lymphoma cells." International Journal of Cancer 120, no. 9 (2007): 2052–57. http://dx.doi.org/10.1002/ijc.22536.

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Barchet, Winfried, Jeffrey D. Price, Marina Cella, Marco Colonna, Sandra K. MacMillan, J. Perren Cobb, Paul A. Thompson, Kenneth M. Murphy, John P. Atkinson, and Claudia Kemper. "Complement-induced regulatory T cells suppress T-cell responses but allow for dendritic-cell maturation." Blood 107, no. 4 (February 15, 2006): 1497–504. http://dx.doi.org/10.1182/blood-2005-07-2951.

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Concurrent activation of the T-cell receptor (TCR) and complement regulator CD46 on human CD4+ T lymphocytes induces Tr1-like regulatory T cells that suppress through IL-10 secretion bystander T-cell proliferation. Here we show that, despite their IL-10 production, CD46-induced T-regulatory T cells (Tregs) do not suppress the activation/maturation of dendritic cells (DCs). DC maturation by complement/CD46-induced Tregs is mediated through simultaneous secretion of GM-CSF and soluble CD40L, factors favoring DC differentiation and reversing inhibitory effects of IL-10. Thus, CD46-induced Tregs produce a distinct cytokine profile that inhibits T-cell responses but leaves DC activation unimpaired. Such “DC-sparing” Tregs could be desirable at host/environment interfaces such as the gastrointestinal tract where their specific cytokine profile provides a mechanism that ensures unresponsiveness to commensal bacteria while maintaining reactivity to invading pathogens.

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Pacholczyk, Rafal, and Joanna Kern. "The T-cell receptor repertoire of regulatory T cells." Immunology 125, no. 4 (December 2008): 450–58. http://dx.doi.org/10.1111/j.1365-2567.2008.02992.x.

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Dissertations / Theses on the topic "Regulatory T cell"

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Carson, Bryan David. "Impaired T cell receptor signaling in regulatory T cells /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8337.

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Stefkova, Martina. "Regulatory T cells control the CD4 T cell repertoire." Doctoral thesis, Universite Libre de Bruxelles, 2016. https://dipot.ulb.ac.be/dspace/bitstream/2013/233151/3/Table.pdf.

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Des études récentes menées chez l’homme et la souris ont suggéré que la diversité du répertoire TCR pourrait jouer un rôle dans la protection contre des pathogènes à haut pouvoir mutagène. Afin d’étudier le répertoire des lymphocytes T CD4, nous avons utilisé un modèle de souris TCRβ transgéniques exprimant une chaine β spécifique du peptide env122-141 dans le contexte du MHCII. Suite à l’immunisation des souris TCRβ transgéniques avec des cellules dendritiques pulsées avec le peptide env, une rapide prolifération et une restriction du répertoire des lymphocytes T Vα2 CD4 spécifiques est observée. L’analyse de la diversité du répertoire de ces cellules par séquençage à haut débit, a montré l’émergence d’un répertoire plus divers dans des souris déplétées en lymphocytes T régulateurs. Ces résultats suggèrent qu’en plus du rôle des Tregs dans le contrôle de la magnitude de la réponse immunitaire, ces cellules pourraient également contrôler la diversité du répertoire des lymphocytes T suite à une stimulation antigénique.
Recent studies conducted in mice and humans have suggested a role for the TCR repertoire diversity in immune protection against pathogens displaying high antigenic variability. To study the CD4 T cell repertoire, we used a mouse model in which T cells transgenically express the TCRβ chain of a TCR specific to a MHCII-restricted peptide, env122-141. Upon immunization with peptide-pulsed dendritic cells, antigen-specific Vα2+ CD4+ T cells rapidly expand and display a restricted TCRα repertoire. In particular, analysis of receptor diversity by high-throughput TCR sequencing in immunized mice suggests the emergence of a broader CDR3 Vα2 repertoire in Treg-depleted mice. These results suggest that Tregs may play a role in the restriction of the CD4 T cell repertoire during an immune response, raising therefore the possibility that in addition to controlling the magnitude of an immune response, regulatory cells may also control the diversity of TCRs in response to antigen stimulation.
Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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Sarris, Milka. "Dynamics of helper T cell and regulatory T cell interactions with dendritic cells." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611896.

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Nadal-Melsio, Elisabet. "Regulatory T cells after allogeneic stem cell transplantation." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.523746.

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Mavin, Emily. "Regulatory T cells in haematopoietic stem cell transplantation." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2731.

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Graft-versus-host disease (GvHD) remains the main complication associated with haematopoietic stem cell transplantation (HSCT). GvHD is caused by allo-reactive donor T cells mounting an attack against specific target tissues. CD4+CD25HiFoxp3+ regulatory T cells have been shown to modulate GvHD in vitro and also in vivo animal models. More recently early stage clinical trials have described the successful use of Treg to reduce the incidence of GvHD following HSCT. The aim of this study was to investigate further the suppressive mechanisms by which Treg are able to modulate GvHD and assess the influence of Treg on the beneficial graft-versus-leukaemia (GvL) effect therefore providing further insight into the use of Treg in the therapeutic management of GVHD. Data presented in this thesis demonstrates the successful isolation and expansion of a highly pure Treg population which maintained suppressive capacity throughout culture. We also confirmed that Treg retain suppressive capacity following cryopreservation resulting in reduced workload and increased consistency when used for in vitro functional studies. We also provide the first human in vitro evidence that Treg are able to prevent cutaneous GvH reaction by blocking the migration of effector T cells into the target tissues. The presence of Treg during allo-stimulation caused reduced effector cell activation, proliferation, IFNγ secretion and decreased skin homing receptor expression. Further investigation into the Treg modulation of dendritic cells demonstrated, for the first time in experimental in vitro human GvHD, that this was due to ineffective effector T cell priming in the presence of Treg caused by impairment of dendritic cell functions. Comprehensive phenotypic and functional analysis of Treg treated moDC showed their decreased antigen processing ability and allostimulatory capacity, resulting in a less severe GvH reaction in the skin explant model. Furthermore, this work has revealed that despite Treg impairing in vitro GvL mechanisms at a cellular level there was no association observed between increased Treg levels and the incidence of relapse in a small clinical cohort of HSCT patients. In conclusion this study has provided further insight into the mechanisms by which Treg are able to modulate GvHD. This would inform future clinical trials using Treg as a therapeutic alternative to current GvHD treatment and prophylaxis.

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Raynor, Jana L. "Regulatory T Cell Homeostasis in Aging." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1416570329.

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Smith, Trevor Robert Frank. "Modulation of CD4+ T cell responses by CD4+CD25+ regulatory T cells and modified T cell epitopes." Thesis, Imperial College London, 2004. http://hdl.handle.net/10044/1/11317.

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Soper, David Michael. "Interleukin-2 receptor and T cell receptor signaling in regulatory T cells /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8344.

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Cabbage, Sarah E. "Reversible regulatory T cell-mediated suppression of myelin basic protein-specific T cells /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/5034.

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Vanderleyden, Ine. "Follicular regulatory T cell migration and differentiation." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288422.

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The germinal centre (GC) response is critical for generating highly effective humoral immune responses and immunological memory that forms the basis of successful immunisation. Control of the output of the GC response requires Follicular regulatory T (Tfr) cells, a subset of Foxp3+ Treg cells located within germinal centres. Tfr cells were first characterised in detail in 2011 and because of this relatively little is known about the exact role of Tfr cells within the GC, and the mechanism/s through which they exert their suppressive function. At the outset of this work, the major barrier to understanding Tfr cell biology was the lack of appropriate tools to study Tfr cells specifically, without affecting Tfh cells or other Treg cell subsets. This thesis set out to develop a strain of mice that specifically lacks Tfr cells. A unique feature of Tfr cells is their CXCR5-dependent localisation within the GC. Therefore, genetic strategies that exclude Treg cells from entering the GC are a rational approach to generating a mouse model that lacks Tfr cells. To this end, I generated a strain of mice that lacks CXCR5 on Foxp3+ Treg cells. These animals show a ~50% reduction in GC localised Tfr cells, and a GC response that is comparable to control animals. These data indicated that redundant mechanisms are involved in Treg cell homing to the GC. I identified CXCR4 as a chemokine receptor that is also highly expressed on Tfr cells, and hypothesised that it may also be involved in Tfr cell localisation to the GC. Surprisingly, simultaneous deletion of both CXCR4 and CXCR5 in Treg cells resulted in a less marked reduction in Tfr cells compared to deletion of CXCR5 alone, suggesting that CXCR4 might be involved in negative regulation of Treg homing to the GC. These data identify both CXCR4 and CXCR5 as key regulators of Tfr cell biology. Bcl6 drives Tfr cell differentiation, but how this transcriptional repressor facilitates commitment to the Tfr cell subset is unknown. I hypothesised that Bcl6 drives Tfr cell differentiation by repressing Tbx21, the transcriptional regulator involved in the differentiation of Th1-like Treg cells. I tested this hypothesis in Bcl6fl/fl CD4cre/+ animals and unexpectedly found that loss of Bcl6 regulates Treg cell differentiation in the absence of immunisation or infection. I have demonstrated that thymic loss of Bcl6 results in an increase in activated effector Treg cells, which occurs very early in life. These data point to a novel role for Bcl6 in preventing early thymic Treg activation, indicating that Bcl6 has a global role in Treg development and differentiation that is not simply limited to Tfr cells.

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Books on the topic "Regulatory T cell"

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Ono, Masahiro, ed. Regulatory T-Cells. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2647-4.

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Kassiotis, George, and Adrian Liston, eds. Regulatory T Cells. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-979-6.

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Taams, Leonie S., Marca H. M. Wauben, and Arne N. Akbar, eds. Regulatory T Cells in Inflammation. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/b137037.

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Jiang, Shuiping, ed. Regulatory T Cells and Clinical Application. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-77909-6.

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Shuiping, Jiang, ed. Regulatory T cells and clinical application. New York: Springer, 2008.

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Regulatory T cells: Methods and protocols. [New York]: Humana Press, 2011.

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Zheng, Song-Guo, ed. T Regulatory Cells in Human Health and Diseases. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-6407-9.

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Compans, R. W., M. D. Cooper, T. Honjo, H. Koprowski, F. Melchers, M. B. A. Oldstone, S. Olsnes, et al., eds. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27702-1.

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Na, Songqing, and Chandrasekar Venkataraman Iyer. Effector CD4+ T cells in health and disease 2007. Kerala, India: Transworld Research Network, 2007.

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R, Bock Gregory, Goode Jamie, and Novartis Foundation, eds. Generation and effector functions of regulatory lymphocytes. Chichester: John Wiley, 2003.

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Book chapters on the topic "Regulatory T cell"

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Sarris, Milka, and Alexander G. Betz. "Live Imaging of Dendritic Cell–Treg Cell Interactions." In Regulatory T Cells, 83–101. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-979-6_7.

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Fowell, Deborah J. "Regulatory T Cell." In Encyclopedia of Medical Immunology, 955–63. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_340.

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Singh, Nagendra, Rafal Pacholczyk, Makio Iwashima, and Leszek Ignatowicz. "Generation of T Cell Hybridomas from Naturally Occurring FoxP3+ Regulatory T Cells." In Regulatory T Cells, 39–44. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-979-6_3.

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Hasenkrug, Kim J., and Lara M. Myers. "In Vitro and In Vivo Analyses of Regulatory T Cell Suppression of CD8+ T Cells." In Regulatory T Cells, 45–54. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-979-6_4.

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Vasconcelos-Fontes, Larissa, Rafaella Ferreira-Reis, João Ramalho Ortigão-Farias, Arnon Dias Jurberg, and Vinicius Cotta-de-Almeida. "Development of Thymic Regulatory T Lymphocytes." In Thymus Transcriptome and Cell Biology, 255–72. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-12040-5_12.

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Damle, Nitin K., Dianne M. Fishwild, Nahid Mohagheghpour, and Edgar G. Engleman. "MHC-Restricted Antigen-Receptor Specific Regulatory T Cell Circuits in Man." In Human T Cell Clones, 197–208. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4998-6_18.

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Hong, Jihye, and Byung-Soo Kim. "Regulatory T Cell-Mediated Tissue Repair." In Advances in Experimental Medicine and Biology, 221–33. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0445-3_14.

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Barcenilla, Hugo, Mikael Pihl, Florence Sjögren, Louise Magnusson, and Rosaura Casas. "Regulatory T-Cell Phenotyping Using CyTOF." In Methods in Molecular Biology, 231–42. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2647-4_15.

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Uhl, Franziska Maria, and Robert Zeiser. "Regulatory T Cells: Broadening Applicability." In Advances and Controversies in Hematopoietic Transplantation and Cell Therapy, 159–77. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-54368-0_9.

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Rüter, Jens, Brian G. Barnett, Ilona Kryczek, Michael J. Brumlik, Benjamin J. Daniel, George Coukos, Weiping Zou, and Tyler J. Curiel. "T-Regulatory Cell Manipulation in Tumor Immunotherapy." In Cancer Vaccines and Tumor Immunity, 189–204. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2007. http://dx.doi.org/10.1002/9780470170113.ch12.

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Conference papers on the topic "Regulatory T cell"

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Velez, T. E., Y. M. Yoon, K. Blaine, C. T. Lee, M. E. Strek, R. Guzy, and A. I. Sperling. "Regulatory T Cell Subsets in Pulmonary Fibrosis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1305.

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Chiang, D., B. Sanjanwala, and KC Nadeau. "Diesel Exhaust Particles Impair Regulatory T Cell Function." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4295.

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Weiss, Vivian L., Timothy H. Lee, Todd D. Armstrong, and Elizabeth M. Jaffee. "Abstract 1923: Regulatory T-cell subsets suppress high avidity CD8 T-cell activation and trafficking." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1923.

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Byrne, William L., Patrick Forde, and Gerald O'Sullivan. "Abstract 5645: Lentiviral-mediated cell-specific RNA interference in regulatory T cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5645.

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Mengistu, D. T., M. S. Toma, M. Busschots, K. Raslan, L. Mccloskey, J. L. Curtis, and C. M. Freeman. "Restoring Regulatory T Cells in COPD Could Dampen Natural Killer Cell Cytotoxicity." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1243.

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Veeramani, Suresh, Sue E. Blackwell, William H. Thiel, Paloma H. Giangrande, and George J. Weiner. "Abstract 5022: Generation of T regulatory-cell specific RNA aptamers." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5022.

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Morales-Nebreda, L., K. Helmin, M. A. Torres Acosta, A. M. Joudi, and B. D. Singer. "Aging Imparts Cell-Autonomous Regulatory T Cell Dysfunction During Recovery from Viral Pneumonia." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1136.

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Hou, Jia, Lei Xin, Junjie Gao, Chengxuan Tian, Weirong Ma, Zhigang Tian, and Xiwei Zheng. "Increased pro-inflammatory regulatory T Cells correlate with the plasticity of T helper cell differentiation in asthma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4993.

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Hsieh, Chyi-Song. "Abstract IA06: Role of TCR specificity in regulatory T cell selection." 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-ia06.

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Griffith, J., L. Faustino, and A. Luster. "Regulatory T Cell Subsets Differentially Regulate the Immune Response to Influenza." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5829.

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Reports on the topic "Regulatory T cell"

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Gray, Andrew. Enhancing the Efficacy of Prostate Cancer Immunotherapy by Manipulating T-Cell Receptor Signaling in Order to Alter Peripheral Regulatory T-Cell Activity. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada511997.

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Gray, Andrew. Enhancing the Efficacy of Prostate Cancer Immunotherapy by Manipulating T-Cell Receptor Signaling in Order to Alter Peripheral Regulatory T-Cell Activity. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada553485.

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Ron, Eliora, and Eugene Eugene Nester. Global functional genomics of plant cell transformation by agrobacterium. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7695860.bard.

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The aim of this study was to carry out a global functional genomics analysis of plant cell transformation by Agrobacterium in order to define and characterize the physiology of Agrobacterium in the acidic environment of a wounded plant. We planed to study the proteome and transcriptome of Agrobacterium in response to a change in pH, from 7.2 to 5.5 and identify genes and circuits directly involved in this change. Bacteria-plant interactions involve a large number of global regulatory systems, which are essential for protection against new stressful conditions. The interaction of bacteria with their hosts has been previously studied by genetic-physiological methods. We wanted to make use of the new capabilities to study these interactions on a global scale, using transcription analysis (transcriptomics, microarrays) and proteomics (2D gel electrophoresis and mass spectrometry). The results provided extensive data on the functional genomics under conditions that partially mimic plant infection and – in addition - revealed some surprising and significant data. Thus, we identified the genes whose expression is modulated when Agrobacterium is grown under the acidic conditions found in the rhizosphere (pH 5.5), an essential environmental factor in Agrobacterium – plant interactions essential for induction of the virulence program by plant signal molecules. Among the 45 genes whose expression was significantly elevated, of special interest is the two-component chromosomally encoded system, ChvG/I which is involved in regulating acid inducible genes. A second exciting system under acid and ChvG/Icontrol is a secretion system for proteins, T6SS, encoded by 14 genes which appears to be important for Rhizobium leguminosarum nodule formation and nitrogen fixation and for virulence of Agrobacterium. The proteome analysis revealed that gamma aminobutyric acid (GABA), a metabolite secreted by wounded plants, induces the synthesis of an Agrobacterium lactonase which degrades the quorum sensing signal, N-acyl homoserine lactone (AHL), resulting in attenuation of virulence. In addition, through a transcriptomic analysis of Agrobacterium growing at the pH of the rhizosphere (pH=5.5), we demonstrated that salicylic acid (SA) a well-studied plant signal molecule important in plant defense, attenuates Agrobacterium virulence in two distinct ways - by down regulating the synthesis of the virulence (vir) genes required for the processing and transfer of the T-DNA and by inducing the same lactonase, which in turn degrades the AHL. Thus, GABA and SA with different molecular structures, induce the expression of these same genes. The identification of genes whose expression is modulated by conditions that mimic plant infection, as well as the identification of regulatory molecules that help control the early stages of infection, advance our understanding of this complex bacterial-plant interaction and has immediate potential applications to modify it. We expect that the data generated by our research will be used to develop novel strategies for the control of crown gall disease. Moreover, these results will also provide the basis for future biotechnological approaches that will use genetic manipulations to improve bacterial-plant interactions, leading to more efficient DNA transfer to recalcitrant plants and robust symbiosis. These advances will, in turn, contribute to plant protection by introducing genes for resistance against other bacteria, pests and environmental stress.

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Wong, Jr, and K. K. Regulatory T Cells and Host Anti-CML Responses. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada487614.

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Wong, Jr, and K. K. Regulatory T Cells and Host Anti-CML Responses. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada510759.

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Lorenz, Ulrike. Role of the Tyrosine Phosphatase SHP-1 and Regulatory T Cells in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada501068.

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Lorenz, Ulrike. Role of the Tyrosine Phosphatase SHP-1 and Regulatory T Cells in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada510570.

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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Abstract:

Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.

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Susurkova, Rumyana, Andrey Velichkov, Antoaneta Mihova, Maria Muhtarova, Matgarita Guenova, Iskra Antonova, Georgi Nikolov, and Velislava Terzieva. Phosphorilated STAT5 Is Associated with Differential Activation Capacity of T Regulatory Cells in Women with Re productive Failure. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, March 2021. http://dx.doi.org/10.7546/crabs.2021.03.15.

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Splitter, Gary, Zeev Trainin, and 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, July 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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