Готові списки джерел за темами / Regulatory T cells; immunology

Добірка наукової літератури з теми "Regulatory T cells; immunology"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 29 січня 2023

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Статті в журналах з теми "Regulatory T cells; immunology"

Simpson, S. J. "IMMUNOLOGY: Animating Regulatory T cells." Science 289, no. 5479 (July 28, 2000): 509a—509. http://dx.doi.org/10.1126/science.289.5479.509a.

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Bluestone, Jeffrey A., and Harald von Boehmer. "Regulatory T cells." Seminars in Immunology 18, no. 2 (April 2006): 77. http://dx.doi.org/10.1016/j.smim.2006.01.003.

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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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Schumacher, Anne, and Ana Claudia Zenclussen. "Regulatory T Cells: Regulators of Life." American Journal of Reproductive Immunology 72, no. 2 (March 24, 2014): 158–70. http://dx.doi.org/10.1111/aji.12238.

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Sakaguchi, Shimon. "Regulatory T cells." Springer Seminars in Immunopathology 28, no. 1 (August 5, 2006): 1–2. http://dx.doi.org/10.1007/s00281-006-0043-2.

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Al Dulaijan, Basmah S., Amr Mansouri, Jordan Karnyski, and Jamil Azzi. "Regulatory T cells." Current Opinion in Organ Transplantation 23, no. 1 (February 2018): 1–7. http://dx.doi.org/10.1097/mot.0000000000000491.

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Allez, Matthieu, and Lloyd Mayer. "Regulatory T Cells." Inflammatory Bowel Diseases 10, no. 5 (September 2004): 666–76. http://dx.doi.org/10.1097/00054725-200409000-00027.

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Garin, Marina I., and Robert I. Lechler. "Regulatory T cells." Current Opinion in Organ Transplantation 8, no. 1 (March 2003): 7–12. http://dx.doi.org/10.1097/00075200-200303000-00003.

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Lui, Prudence PokWai, Inchul Cho, and Niwa Ali. "Tissue regulatory T cells." Immunology 161, no. 1 (June 24, 2020): 4–17. http://dx.doi.org/10.1111/imm.13208.

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Maggi, Enrico, Lorenzo Cosmi, Francesco Liotta, Paola Romagnani, Sergio Romagnani, and Francesco Annunziato. "Thymic regulatory T cells." Autoimmunity Reviews 4, no. 8 (November 2005): 579–86. http://dx.doi.org/10.1016/j.autrev.2005.04.010.

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Дисертації з теми "Regulatory T cells; immunology"

Lindqvist, Camilla. "T Regulatory Cells – Friends or Foes?" Doctoral thesis, Uppsala universitet, Enheten för klinisk immunologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-128837.

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T regulatory cells (Tregs) have been extensively studied in patients with cancer or autoimmunity. These cells hamper the immune system’s ability to clear tumor cells in cancer patients. In autoimmune diseases, on the other hand, they are not able to restrain autoreactive immune responses. If we manage to understand Tregs and their role in health and diseases we may be able to develop better immunomodulatory therapies. Early studies demonstrated that tolerance was maintained by a subset of CD25+ T-cells. CD25 was the earliest marker for Tregs and is still often used to define these cells. Several Treg-associated markers have been suggested throughout the years. However, these markers can be upregulated by activated T-cells as well. The most specific marker for Tregs is currently the transcription factor forkhead box P3 (FoxP3). In this thesis, we investigated the presence of CD25- Tregs in patients with B-cell malignancies and in patients with autoimmunity. These cells were identified in both patient groups. Further, patients with B-cell malignancies often have high levels of soluble CD25 (sCD25) in the periphery. In our patient cohorts, the level of peripheral Tregs correlated with the level of sCD25 in patients with lymphoma. Tregs were shown to release sCD25 in vitro and sCD25 had a suppressive effect on T-cell proliferation. These data show that Tregs may release CD25 to hamper T-cell proliferation and that this may be an immune escape mechanism in cancer patients. Previous studies have demonstrated that an increased infiltration of FoxP3+ cells into lymphoma-affected lymph nodes is associated with a better patient outcome. This is in contrast to studies from non-hematological cancers where an increased presence of Tregs is associated with a poor prognosis. Since previous studies have shown that Tregs are able to kill B-cells, we wanted to investigate if Tregs are cytotoxic in patients with B-cell tumors. In the subsequent studies, Tregs from patients with B-cell lymphoma and B-cell chronic lymphocytic leukemia (CLL) were phenotyped to investigate the presence of cytotoxic markers on these cells. FoxP3-expressing T-cells from both patients with CLL and B-cell lymphoma displayed signs of cytotoxicity by upregulation of FasL and the degranulation marker CD107a. Tregs from CLL patients could further kill their autologous B-cells in in vitro cultures. Taken together the studies in this thesis have demonstrated two possible new functions of Tregs in patients with B-cell malignancies and the presence of CD25- Tregs in both cancer and autoimmunity.

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Sayin, Ismail. "Characterization of human T follicular regulatory cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1560336991188191.

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Emani, Sirisha. "MOLECULAR CHARACTERIZATION OF T REGULATORY CELLS IN FIV-INFECTION." NCSU, 2006. http://www.lib.ncsu.edu/theses/available/etd-01192006-105756/.

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Naturally occurring CD4+CD25+ T regulatory cells (Treg) play important roles in maintaining immunologic self-tolerance in addition to controlling the magnitude of anti-microbial immune responses. However, the capacity of these CD4+CD25+ Treg cells to control immune responses both in vivo and in vitro is not well established. CD4+CD25+ Treg cell-mediated suppression can control autoimmune diseases; transplantation tolerance and graft verses host disease and, in contrast hinder tumor immunity and immunity to infectious agents. As Treg cells have been reported to be involved in several diseases, this study focused on molecular characteristics that enables them to maintain anergy and also resistance to programmed cell death along with the effect of FIV-infection on regulation of the above phenotypic characteristics. Our results show that feline CD4+CD25+ Treg cells are phenotypically and functionally anergic as indicated by elevated levels of the cyclin dependent kinase inhibitors, CdkI¡¦s, (p21cip1,p16ink4, and p27kip1) , and resistance to mitogen-induced proliferation compared to their counter parts CD4+CD25- T cells. Importantly, CdkI¡¦s are constitutively over-expressed only in FIV-infected cats. As expected Treg cells from FIV-infected cats that over-expressed CdkI¡¦s expressed low levels of the cyclins (mainly cyclins D) and phosphorylated retinoblastoma protein (pRb) that are responsible for cell cycle progression. We investigated the role of TGF?Ò signaling and found that TGF?Ò1 plus ConA stimulation was able to convert CD4+CD25- T cells to CD4+CD25+ T cells with functional and phenotypic characteristics including upregulation of CdkI¡¦s and bcl-2. The differential expression of CdkI¡¦s and bcl-2 between the two CD4+ T cell subsets may be linked to TGF?Ò-Smad pathway. Consistent with upregulation of CdkI¡¦s and bcl-2, we found that although natural and TGF?Ò1 converted CD4+CD25+ Treg cells are anergic, they are more resistant to activation induced cell death compared to CD4+CD25- T cells functionally which correlated with increased bcl-2 to bax ratio in Treg cells. Thus, the molecular characterization of this unique population of Treg cells may be essential for understanding their role and function for developing effective therapeutics and vaccination especially against chronic infections such as Acquired Immune Deficiency Syndrome (AIDS).

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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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Chen, Ye. "Induced regulatory T cells in transplantation tolerance." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:cffc275b-d32c-495e-a1da-55421a57e7e7.

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Induced regulatory T cells (iTreg) play an important role in the induction of tolerance to self and non-self antigens. Harnessing their suppressive potential has therapeutic implications for the treatment of autoimmune conditions and transplant rejection. Although the role of TGFβ-conditioned iTreg in natural and therapeutic tolerance is indisputable, their mechanism of action as well as factors that influence their function and stability in vivo remain unclear. Here it is shown that TGFβ-conditioning of T cells in the absence of any Foxp3 expression is insufficient for conferring a suppressive phenotype in vivo, whilst Foxp3 expression is sufficient to enable naïve T cells to become suppressive both in vitro and in vivo. Graft antigen was found to enhance the number of iTreg-derived Foxp3+ cells localising to the draining lymph nodes of recipients, and this was associated with histone modifications at the Foxp3 locus that suggested a stabilisation or 'affirmation' of Foxp3 expression. Finally, iTreg were shown to 'out-compete' naïve T cells in forming clusters with dendritic cells. Activated inflammatory T cells could also 'out-compete' naïve T cells. However, unlike activated T cells, iTreg did not activate interacting DCs to the same extent, and this may potentially be a mechanism of their action in vivo.

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Alexander, Carla-Maria Alana. "T regulatory cells and the germinal center." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/1117.

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Germinal center (GC) reactions are central features of T cell-driven B cell responses, and the site where antibody (Ab) producing cells and memory B cells are generated. Within GCs, a range of complex cellular and molecular events occur which are critical for the generation of high affinity Abs. These processes require exquisite regulation not only to ensure the production of desired Abs, but to minimize unwanted autoreactive or low affinity Abs. To assess whether T regulatory cells (Treg) participate in the control of GC responses, immunized mice were treated with either an anti-glucocorticoid-induced TNFR-related protein (GITR) mAb or an anti-CD25 mAb to disrupt Treg activity. In both groups of treated mice, the GC B cell pool was significantly larger compared with control treated animals, with switched GC B cells composing an abnormally high proportion of the response. With these results indicating Tregs influence on GC dynamics, experiments were conducted to determine if Tregs were located in the GC, which subset of Treg was involved and by which mechanisms were their functions being effected. Within the spleens of immunized mice, CXCR5+ and CCR7- Tregs were documented by flow cytometry and Foxp3+ cells were found within GCs using immunohistology. Studies demonstrated administration of either anti-TGF-β or anti-IL-10R blocking mAb to likewise result in dysregulated GCs, suggesting that generation of inducible Tregs is important in controlling the GC response. Blockade of two Treg methods of suppression, PD-1/PD-L1 pathway and CTLA-4, also resulted in disrupted GCs, indicating the possible use of them for suppression by Treg. Collectively, these findings indicate that Tregs contribute to the overall size and quality of the humoral response by controlling homeostasis within GCs.

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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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Okeke, Emeka B. "Regulation of Sepsis and Endotoxic Shock by Regulatory T cells." Wolters Kluwer Health Lippincott Williams & Wilkins, 2013. http://hdl.handle.net/1993/31580.

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One of the major challenges facing clinicians is how to effectively manage excessive host immune response to pathogenic insults resulting in sepsis. This is demonstrated by the fact that despite over half-century research efforts, sepsis and its spectrum of diseases (severe sepsis and septic shock) are still associated with poor clinical outcome. Currently, sepsis is a leading cause of death in intensive care units. The immune system protects the host against pathogens and is therefore armed with an arsenal of deadly ammunitions (including chemicals, cells and proteins) necessary for the elimination of microbes. It is therefore paramount that the immune system must develop mechanisms necessary to prevent destruction of the host it is designed to protect. A good example of such a mechanism is found in the subset of lymphocytes known as regulatory T cells (Tregs). There is unequivocal experimental evidence of the role of Tregs in the maintenance of immune homeostasis and self tolerance and aberrant Treg function has been linked with several inflammatory diseases. Since sepsis is a disease marked by a hyper-inflammatory state, I investigated the possible role of Tregs in dampening sepsis-induced excessive inflammation. Using a murine model of lipopolysaccharide (LPS) infusion and bacterial infection, I show that Tregs are essential for survival during sepsis because their depletion leads to acute death to an otherwise non-lethal dose of LPS. This enhanced susceptibility to LPS following Treg depletion was also observed using live E. coli infection. Next, I probed the mechanism by which Tregs protect against LPS challenge. I found that defective Treg function leads to exaggerated activity of two immune cells – CD4+ effector T cells and neutrophils in response to LPS, leading to severe inflammatory response. Hence, this work successfully illustrates the critical role of Tregs in regulating other immune cells and the catastrophic consequences of defective Treg function during an immune response. Overall, this work highlights the significant role of Tregs in the regulation of bacteria associated inflammatory processes. The findings hold implications for the successful management of sepsis and have potential for use in development of adequate therapeutic intervention for sepsis.
October 2016

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Chatila, Wissam M. "MicroRNA expression in regulatory T cells in chronic obstructive pulmonary disease." Thesis, Temple University, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=3719335.

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COPD is characterized by an abnormal regulatory T cell (Treg) response with a shift towards a Th1 and Th17 cell responses. However, it is unclear if the function of Treg cells is impaired by smoking and in COPD. In addition, the miRNA profile of Treg cells in COPD is unknown and whether miRNA deregulation contributes to COPD immunopathogenesis. We set the objective to study Treg cell function isolated from peripheral blood of patients with COPD versus controls and to compare their miRNA profiles. We also were interested in exploring the function of some of the differentially expressed Treg cell miRNAs. We assessed the Treg cell function by observing their suppressive activity on autologous effector T cells and analyzed their miRNA expression initially by microarray analysis then conducted real time RT-PCR validation for selected miRNAs. In Silico target gene analysis for the validated miRNAs suggested that miR-199-5p is particularly relevant to Treg cell physiology so its function was investigated further using CCD-986Sk and MOLT-4 cells. We found no difference in Treg cell function between COPD and controls but we were able to identify 6 and 96 miRNAs that were differentially expressed in COPD versus control Treg cells. We confirmed that miR-199a-5p was repressed by approximately 4 fold in Treg cells of COPD patients compared to cells in healthy smokers. Importantly, miR-199a-5p had significant overrepresentation of its target genes in the Treg cell transcriptome, with many targets associated with the TGF-β activation pathway. We also confirmed the function of miR-199a5p in an in-vitro loss-of-function cell model running TaqMan® arrays of the Human TGF-β Pathway. These findings suggest that the abnormal repression of miR-199a-5p in patients with COPD compared to unaffected smokers may be involved in modulating the adaptive immune balance in favor of a Th1 and Th17 response.

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Lee, Crystal. "Suppressive activity of CD4+Foxp3+ regulatory T cells in an animal model of spontaneous CD8+ T cell-mediated demyelinating disease." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110761.

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Dr. Fournier's laboratory has generated a mouse strain (L31 mice) that spontaneously develops a CD8+ T cell-mediated demyelinating disease in the central nervous system. In this model of dysregulated costimulation, CD4+ T cells have a regulatory role. A subset of CD4+ regulatory T cells that express the transcription factor Foxp3 have been shown to regulate autoimmune responses. In order to investigate this population's role in disease development, the goal of my M.Sc research project was to functionally characterize the CD4+Foxp3+ regulatory T cell population in L31 mice.We found that regulatory T cells from L31 mice were impaired in their ability to suppress the proliferation of effector T cells in vitro. In part, this was because B7.2 (CD86) expression impeded regulatory T cell suppressive activity. However, regulatory T cells delayed the onset of neurological symptoms in vivo. Although L31 Treg are not suppressive in vitro, our in vivo data suggest that they have a regulatory function in L31 disease development. This dichotomy could provide insights into the mechanisms by which these regulatory T cells control disease development in L31 mice.
Le laboratoire du Dr. Fournier a généré une lignée de souris (les souris L31) qui développe de façon spontanée une maladie du système nerveux central qui conduit à la perte de la gaine de myéline et qui est dépendante de la presence de lymphocytes T. Dans ce modèle les lymphocytes CD8+ sont les cellules effectrices de la maladie tandis que les lymphocytes T CD4+ jouent un rôle régulateur. Il a été démontré qu'une sous-population de lymphocytes T CD4+ qui expriment le facteur de transcription Foxp3 est impliquée dans la regulation des réponses auto-immunes. Afin d'étudier le rôle de cette population dans le développement de la maladie neurologique des souris L31, le but de mon projet de recherche était de caractériser de façon fonctionelle cette sous-population de lymphocytes T CD4+ régulateurs des souris L31. Nous avons trouvé que les lymphocytes T régulateurs des souris L31 sont altérés dans leur capacité à supprimer la proliferation de cellules T effectrices in vitro. Ceci est dû en partie à leur expression elevée de la protein B7.2 (CD86). Cependant, les lymphocytes T régulateurs des souris L31 sont capables de prévenir le développement des symptômes neurologiques in vivo. Donc, bien que les lymphocytes T régulateurs des souris L31 ne sont pas suppresseurs in vitro, notre données in vivo suggèrent qu'ils ont une fonction régulatrice dans le développement de la maladie neurologique des souris L31. Cette dichotomie pourrait nous permettre de déterminer les mécanismes utilisés par ces cellules régulatrices pour contrôler le développement de la maladie neurologique auto-immune dans les souris L31.

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Книги з теми "Regulatory T cells; immunology"

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

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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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I, Gabrilovich Dmitry, and Hurwitz Arthur A, eds. Tumor-induced immune suppression: Mechanisms and therapeutic reversal. New York, NY: Springer, 2008.

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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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Marc, Feldmann, Lamb Jonathan R, and Owen M. J, eds. T cells. New York: Wiley, 1989.

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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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Zanetti, M. Memory T cells. New York: Springer Science+Business Media, 2010.

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Debré, P. Clonage des lymphocytes T. Paris: Societé française d'immunologie, 1989.

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Частини книг з теми "Regulatory T cells; immunology"

Gawlik, Barbara B., and David A. Hafler. "Regulatory T Cells in MS." In Multiple Sclerosis Immunology, 27–47. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7953-6_2.

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Brunner, M. C., D. Caput, M. R. Helbert, N. A. Mitchison, K. Simon, J. Sieper, and P. Wu. "Regulation of Regulatory T Cells." In Progress in Immunology Vol. VIII, 613–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_79.

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Kim, Chang H. "Regulatory T-Cells and Th17 Cells in Tumor Microenvironment." In Cancer Immunology, 91–106. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30845-2_6.

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Kim, Chang H. "Regulatory T Cells and Th17 Cells in Cancer Microenvironment." In Cancer Immunology, 77–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44006-3_6.

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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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Pucino, Valentina, Veronica De Rosa, Claudio Procaccini, and Giuseppe Matarese. "Regulatory T Cells, Leptin and Angiogenesis." In Chemical Immunology and Allergy, 155–69. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000353557.

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Massoud, Amir Hossein. "Age-Related Alterations in Regulatory T Cells." In Immunology of Aging, 201–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-39495-9_13.

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Enders, G. A. "Regulatory T Cells in the Galt." In Recent Advances in Mucosal Immunology, 149–54. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_17.

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Kretschmer, Karsten, Irina Apostolou, Panos Verginis, and Harald von Boehmer. "Regulatory T Cells and Antigen-Specific Tolerance." In Chemical Immunology and Allergy, 8–15. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000154846.

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Strickland, Deborah H., Matthew E. Wikstrom, Debra J. Turner, and Patrick G. Holt. "Mucosal Regulatory T Cells in Airway Hyperresponsiveness." In Chemical Immunology and Allergy, 40–47. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000154855.

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Тези доповідей конференцій з теми "Regulatory T cells; immunology"

Li, Amy, Arjun Bhutkar, Nikhil S. Joshi, and Tyler E. Jacks. "Abstract A66: Molecular profiling of regulatory T cells in a genetic mouse model of lung adenocarcinoma." 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-a66.

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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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Noël, Grégory, Mireille Langouo, Soizic Garaud, Anaïs Boisson, Hugues Duvillier, Gert Van den Eynden, Denis Larsimont, and Karen Willard-Gallo. "Abstract A40: The balance between activated follicular helper T cells and follicular regulatory T cells within tertiary lymphoid structures guides antitumor immune responses in human breast cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a40.

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Ward, Stephen T., Elizabeth A. Hepburn, Ka-kit Li, Stuart M. Curbishley, Rahul K. Hejmadi, Tariq Ismail, Roy Bicknell, Antal Rot, and David H. Adams. "Abstract A73: The selective recruitment and retainment of regulatory T cells in human colorectal cancer." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a73.

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Shahoei, Sayyed Hamed, Adam T. Nelson, Madeline A. Henn, Ashley E. Mathews, Joy J. Chen, Varsha Vembar, Liqian Ma, Lionel Apetoh, and Erik R. Nelson. "Abstract A93: Macrophage-expressed small heterodimer partner impairs expansion of regulatory T cells and enhances immune checkpoint inhibition." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a93.

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Song, Qing-Kun, Jun Ren, Xiao-Li Wang, Xin-Na Zhou, Hua-Bing Yang, Yu-Chen Li, and Jiang-Ping Wu. "Abstract B14: CD4+CD25+ regulatory T lymphocytes: Prognostic indicator of Chinese breast cancer patients receiving dentitric cells-cytokine induced killer cells infusion." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b14.

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Das, Satya N., Sadhna Aggarwal, and Suresh C. Sharma. "Abstract A67: Phenotypic and functional dynamics of CD4+CD25+FOXP3+ regulatory T cells in patients with tobacco-related oral squamous cell carcinoma." 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-a67.

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Zhang, Hongru, Jun Gui, Angelica Ortiz, and Serge Fuchs. "Abstract A100: Downregulation of type 1 interferon receptor (IFNAR1) regulates the balance of regulatory T cells (Tregs) and cytotoxic T lymphocytes (CTLs) in tumor microenvironment." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a100.

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Park, Chan Kwon, and Seung Joon Kim. "Abstract B70: Differential expression of regulatory T cells and Th17 cells are indicative of tumor recurrence in pN0 stage I lung cancer patients." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-b70.

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Hope, Jennifer L., Dennis C. Otero, Eun-ah Bae, Christopher J. Stairiker, Ashley B. Palete, Hannah A. Faso, Petrus de Jong, Garth Powis, and Linda M. Bradley. "Abstract PO014: PSGL-1 is an early T cell signaling regulator that drives immunometabolism and terminal differentiation in tumor-specific CD8 T cells." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po014.

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Звіти організацій з теми "Regulatory T cells; immunology"

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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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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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Анотація:

Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.

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