Relevant bibliographies by topics / Murine T Cells

Academic literature on the topic 'Murine T Cells'

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Published: 18 May 2024

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Journal articles on the topic "Murine T Cells"

1

Gaur, Amitabh. "Cloning of Murine T Cells." Methods 9, no. 3 (June 1996): 411–15. http://dx.doi.org/10.1006/meth.1996.0046.

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Sato, Katsuaki, Naohide Yamashita, Masanori Baba, and Takami Matsuyama. "Modified myeloid dendritic cells act as regulatory dendritic cells to induce anergic and regulatory T cells." Blood 101, no. 9 (May 1, 2003): 3581–89. http://dx.doi.org/10.1182/blood-2002-09-2712.

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To exploit a novel strategy to regulate T cell–mediated immunity, we established human and murine modified dendritic cells (DCs) with potent immunoregulatory properties (designed as regulatory DCs), which displayed moderately high expression levels of major histocompatibility complex (MHC) molecules and extremely low levels of costimulatory molecules compared with their normal counterparts. Unlike human normal DCs, which caused the activation of allogeneic CD4+ and CD8+ T cells, human regulatory DCs not only induced their anergic state but also generated CD4+ or CD8+regulatory T (Tr) cells from their respective naive subsets in vitro. Although murine normal DCs activated human xenoreactive T cells in vitro, murine regulatory DCs induced their hyporesponsiveness. Furthermore, transplantation of the primed human T cells with murine normal DCs into severe combined immunodeficient (SCID) mice enhanced the lethality caused by xenogeneic graft-versus-host disease (XGVHD), whereas transplantation of the primed human T cells with murine regulatory DCs impaired their ability to cause XGVHD. In addition, a single injection of murine regulatory DCs following xenogeneic or allogeneic transplantation protected the recipients from the lethality caused by XGVHD as well as allogeneic acute GVHD. Thus, the modulation of T cell–mediated immunity by regulatory DCs provides a novel therapeutic approach for immunopathogenic diseases.
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Craft, Joe, Stanford Peng, Takao Fujii, Masato Okada, and Saeed Fatenejad. "Autoreactive T cells in murine lupus." Immunologic Research 19, no. 2-3 (June 1999): 245–57. http://dx.doi.org/10.1007/bf02786492.

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Adkins, Becky, and Mehdi Nassiri. "Apoptosis of Murine Neonatal T Cells." International Reviews of Immunology 18, no. 5-6 (January 1999): 465–84. http://dx.doi.org/10.3109/08830189909088494.

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Mally, Martin I., Marguerite Vogt, Susan E. Swiftt, and Martin Haas. "Oncogene expression in murine splenic T cells and in murine T-Cell neoplasms." Virology 144, no. 1 (July 1985): 115–26. http://dx.doi.org/10.1016/0042-6822(85)90310-1.

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Hayakawa, K., and R. R. Hardy. "Murine CD4+ T cell subsets defined." Journal of Experimental Medicine 168, no. 5 (November 1, 1988): 1825–38. http://dx.doi.org/10.1084/jem.168.5.1825.

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We have used two monoclonal anti-murine T cell autoantibodies (SM3G11 and SM6C10) and multi-color immunofluorescence staining to resolve splenic CD4+ cells into four populations. Two of these populations (Fr. I and Fr. III, 35% and 10% of CD4+ cells) show mutually exclusive expression of these determinants and exhibit distinct functions. Fr. III secretes IL-4, but not IL-2 when activated by Con A, and includes memory T cells responsible for secondary antibody formation. In contrast, Fr. I secretes IL-2 but not IL-4 in response to Con A, and does not contribute to the secondary antibody response. Furthermore, these two fractions exhibit differential accessory cell dependence. Whereas Fr. III responds with B cells (and also non-B cells) as accessory cells in Con A-induced activation, Fr. I requires non-B cells. However, we found that many CD4+ cells (Fr. II, 40% of CD4+ cells) express both determinants and are not distinguishable with regard to lymphokine secretion, accessory cell effect, and memory T cell activity. Curiously, the fraction expressing neither determinant (Fr. IV, 10% of CD4+ cells) is unresponsive to experimental conditions used here. We discuss the possible relationships between these T cell subsets and the implications of differential expression of these determinants.
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Lucas, P. J., C. V. Bare, and R. E. Gress. "The human anti-murine xenogeneic cytotoxic response. II. Activated murine antigen-presenting cells directly stimulate human T helper cells." Journal of Immunology 154, no. 8 (April 15, 1995): 3761–70. http://dx.doi.org/10.4049/jimmunol.154.8.3761.

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Abstract Generation of a human T cell anti-murine xenogeneic response has previously been shown to be dependent on presentation of murine Ag by human APC. We have undertaken a series of experiments to better delineate the cellular defects that prevent effective production of IL-2 by human T cells upon direct exposure to murine stimulator populations. It was found that although resting human T cells cannot respond effectively to resting murine APC, they can respond to activated murine stimulator populations. Such APC activation could be mediated by murine granulocyte-macrophage-CSF or LPS that were associated with increased expression of B7-2 on the xenogeneic stimulating cell populations. Blocking studies with Ab provided further evidence that costimulation through CD28 played a critical role in the stimulation of human T cells by activated murine-stimulator cells in the production of IL-2. These results demonstrate the usefulness of this xenogeneic system in understanding human T cell-APC interactions and defining minimally sufficient T cell activation requirements. They further delineate the cellular level of deficient activation in the xenogeneic stimulation of human T cells by murine cell populations, and identify the potential importance of CD28/CTLA4 and its ligands in xenogeneic responses. These observations and concepts have implications for clinical efforts in xenografting.
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Baars, Paul A, Sophie Sierro, Ramon Arens, Kiki Tesselaar, Berend Hooibrink, Paul Klenerman, and René A W. van Lier. "Properties of murine CD8+CD27- T cells." European Journal of Immunology 35, no. 11 (November 2005): 3131–41. http://dx.doi.org/10.1002/eji.200425770.

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Du, Jing, Katelyn Paz, Govindarajan Thangavelu, Dominik Schneidawind, Jeanette Baker, Ryan Flynn, Omar Duramad, et al. "Invariant natural killer T cells ameliorate murine chronic GVHD by expanding donor regulatory T cells." Blood 129, no. 23 (June 8, 2017): 3121–25. http://dx.doi.org/10.1182/blood-2016-11-752444.

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Algood, Holly M. Scott, Victor J. Torres, Derya Unutmaz, and Timothy L. Cover. "Resistance of Primary Murine CD4+ T Cells to Helicobacter pylori Vacuolating Cytotoxin." Infection and Immunity 75, no. 1 (October 30, 2006): 334–41. http://dx.doi.org/10.1128/iai.01063-06.

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ABSTRACT Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for the development of gastric cancer and peptic ulcer disease. H. pylori secretes a toxin, VacA, that targets human gastric epithelial cells and T lymphocytes and enhances the ability of H. pylori to colonize the stomach in a mouse model. To examine how VacA contributes to H. pylori colonization of the mouse stomach, we investigated whether murine T lymphocytes were susceptible to VacA activity. VacA inhibited interleukin-2 (IL-2) production by a murine T-cell line (LBRM-33), similar to its effects on a human T-cell line (Jurkat), but did not inhibit IL-2 production by primary murine splenocytes or CD4+ T cells. VacA inhibited activation-induced proliferation of primary human CD4+ T cells but did not inhibit the proliferation of primary murine CD4+ T cells. Flow cytometry studies indicated that the levels of VacA binding to primary murine CD4+ T cells were significantly lower than levels of VacA binding to human CD4+ T cells. This suggests that the resistance of primary murine CD4+ T cells to VacA is attributable, at least in part, to impaired VacA binding to these cells.
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Dissertations / Theses on the topic "Murine T Cells"

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Paun, Andrea. "Regulator T cells in murine AIDS." University of Western Australia. Microbiology and Immunology Discipline Group, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0115.

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[Truncated abstract] In the last ten years regulator T (Tr) cells have re-emerged as an integral part of the immune system. Research in this field has rapidly demonstrated the role of these cells in the maintenance of immune homeostasis and their involvement in disease. Tr cells are generated in the thymus as a normal part of the developing immune system. Furthermore, antigen-specific Tr cells are induced in the periphery by a mechanism which is yet to be completely elucidated, but is likely to involve dendritic cells. Tr cells play an important role in autoimmune disease, transplantation tolerance, cancer. Most recently Tr cell involvement has been demonstrated in a growing number of infectious diseases. Tr cell induction was reported in Friend Virus infection at the commencement of this study, and subsequent to publication of our findings have also been identified in FIV and HIV. Murine AIDS (MAIDS) is a fatal chronic retroviral infection induced in susceptible strains of mice by infection with BM5d, a replication defective virus, in a viral mixture which is designated LP-BM5. The manipulation of Tr cells detailed in this thesis and the related publication represent the first reported therapy utilising targeted removal of Tr cells. Chapter 1 summarises the literature relevant to this study up to November 2004. Chapter 2 details the materials and methodologies used in this work. Chapter 3 investigates whether Tr cells are involved in the development of murine AIDS, particularly in the early stages of infection. The data presented in this chapter provides evidence of a population of CD4+ Tr cells which express CD25 on their cell surface and secrete TGF-β, some IL-10 and low levels of IL-4 are induced following infection with LP-BM5. These cells were found to arise by day 12 post infection (pi) by flow cytometry and immunosuppressive cytokine expression was found to peak at day 16 pi indicating a role in the early stages of disease progression. Chapter 4 investigates the effect of therapeutically targeting these induced Tr cells using the antimitotic agent Vinblastine during their induction period. The efficacy of treatment was found to be time dependent and was shown to abrogate disease progression maximally when given at day 14 pi. Treatment with anti-CD4 monoclonal antibody was also found to be efficacious at day 14 pi and confirmed the identity of the Tr cells as being CD4+ T cells. Adoptive transfer studies demonstrated that the return of these cells to a successfully treated host results in renewed MAIDS progression, confirming their role in disease progression
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Podrebarac, Theresa A. "CD1 restricted recognition by murine T cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ46602.pdf.

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Hughes, Jane Patricia. "Molecular regulation of apoptosis in immature murine T-cells." Thesis, Keele University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301341.

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Belfrage, Hans. "Activation of murine cytotoxic cells with interleukin-2 and the bacterial superantigen staphylococcal enterotoxin A." Lund : Dept. of Cell & Molecular Biology, Section of Tumor Immunology, the Wallenberg Laboratory, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38037867.html.

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Garefalaki, Anna. "Identification of regulatory regions that determine expression of murine CD8 locus." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250198.

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Chan, Agnes How-Ching. "Purification, biochemical analysis and sequencing of a novel murine T suppressor factor." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28638.

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The work reported in this thesis involved the purification, biochemical analysis and sequencing of a novel suppressor factor secreted by a T cell hybridoma, A10. The factor, A10F, isolated from spent medium of A10 cells, was found to consist of two forms with molecular weights at 140 - 160 and 80 kD as suggested by NH₂-terminal sequencing, Western blotting and tryptic peptide mapping experiments. Both forms of A10F were found to be capable of suppressing the in vitro generation of cytotoxic T lymphocyte (CTL) specific for P815 cells by syngeneic (DBA/2) splenocytes. In vitro ³⁵S methionine labeling experiments clearly demonstrated that the 80 kD protein was a secretory product of the A10 cells. The protein, which was specific to the monoclonal antibody (B16G), was absent in the control NS1 and BW5147 cells. Biochemical analysis indicated that the 80 kD molecule, was either a degradation product or a monomer of the 140 - 160 kD molecule. Further degradation products such as the 32 kD molecules were also found. This peptide, however, did not seem to cause substantial suppression in the in vitro CTL assay. When the 140 - 160, 80 and 32 kD proteins were sequenced at the NH₂ terminus, both 140 - 160 and 80 kD proteins were found to possess the same NH₂ terminus sequence. The 32 kD protein, on the other hand, was found to have an NH₂-terminus quite different from that of the 80 kD protein. These findings suggested that the 32 kD fragment was probably located at the distal end of the 140 - 160 kD molecule.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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Tomkins, Paul Thomas. "Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells." Thesis, University of Warwick, 1989. http://wrap.warwick.ac.uk/101165/.

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Cultures of astrocytes prepared from the brains of newborn mice, G26-24 oligodendroglioma cells and C1300 neuroblastoma cells were treated with Interferon (IFN) and the effect on major histocompatibility complex (MHC) antigen expression assessed by indirect immunofluorescence. IFN-αβ increased class I, but not class II, MHC antigen expression on astrocytes, G26-24 cells and C1300 cells. IFN-β1, increased class I, but not class II, MHC antigen expression on astrocytes. IFN-γ increased both class I and class II MHC antigen expression on astrocytes and G26-24 cells. IFN-γ increased class I, but not class II, MHC antigen expression on C1300 cells. IFN-αβ and IFN-β were additive with IFN-γ in the induction of class I MHC antigen expression on astrocytes, but inhibited the ability of IFN-γ to induce class II MHC antigen expression. IFN-αβ and IFN-γ increased the susceptibility of astrocytes, C26-24 cells and C1300 cells to lysis by alloreactive cytotoxic T-lymphocytes (CTL) indicating that IFNs increased the ability of the cells to participate in class I MHC restricted T-cell immune reactions. Astrocytes treated with IFN-αβ or IFN-γ, and G26-24 cells and C1300 cells treated with IFN-γ, prior to infection with Semliki Forest virus (SFV), showed a similar or increased susceptibility to SFV-specific CTL lysis, despite a reduction of SFV antigen display on the cells, as assessed by indirect immunofluorescence and susceptibility to lysis by anti-SFV antibody plus complement. It is concluded that even when SFV antigen expression is reduced by IFN treatment, in the context of enhanced class I MHC antigen expression cells remain susceptible to SFV-specific CTL lysis. IFN-αβ and IFN-γ treatment of astrocytes, and IFN-γ treatment of G26-24 cells, prior to treatment with a β-propiolactone inactivated preparation of SFV, increased the ability of the cells to stimulate SFV-specific T-cell release of IFN-γ. This increased ability correlated with an increase in MHC antigen expression on the cells. IFN-γ released by SFV-specific T-cells increased class I and class II MHC antigen expression on astrocytes and G26-24 cells indicating that a positive feedback mechanism could operate. SFV-infected newborn and adult mice possessed high levels of IFN-αβ in the brain. Brain extracts prepared from SFV-infected newborn and adult mice increased class I, but not class II, MHC antigen expression on astrocytes in vitro. Class I and class II MHC antigen expression was slightly elevated in the brains of SFV-infected newborn mice. To study the role of endogenous IFN-γ, R4-6A2 anti-IFN-γ monoclonal antibody was administered to adult mice, prior to infection with SFV, and the effect on the clinical course of SFV-disease monitored. R4- 6A2 antibody had no effect and preliminary experiments indicated that the antibody may not neutralise all IFN-γ activity in vivo under the conditions used.
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Chan, Po-Ying. "Characterization and cDNA cloning of a novel murine T cell surface antigen YE1/48." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28640.

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T cell surface antigens are thought to play significant roles in immunological functions. They are involved in cellular interactions and T cell activation and proliferation. Characterization of T cell antigens is important in understanding the molecular machanisms underlying immune responses. The subject of this thesis is to characterize a novel murine T cell surface antigen called YE1/48. YE1/48, defined by two rat monoclonal antibodies YE1/48.10.6 and YE1/32.8.5, is a dimeric glycoprotein with molecular size and charge resembling the murine T cell antigen receptor α/β. It was initially detected at high levels on two T cell lymphomas, EL-4 and MBL-2. In my thesis studies, the YE1/48 antigen was characterized biochemically, a cDNA clone was isolated, and its expression in lymphoid cell populations was determined. The YE1/48 antigen was found to be distinct from the T cell receptor based on direct comparisons of their primary sequences as well as immunological analyses. It is likely a homodimer with similar or identical subunits. No homology with any known proteins could be detected, including the human T cell activation antigen CD28 (T44) which also has a similar dimeric structure as YE1/48. No function of the YE1/48 antigen could be derived from its primary sequence or with the use of the two monoclonal antibodies because the antibodies do not appear to bind to the surface of intact normal T lymphocytes. Some intriguing characteristics of the YE1/48 antigen were observed in the current studies. The YE1/48 antigen belongs to a rare group of type II membrane proteins with orientation of the amino-terminus inside the cell and the carboxy-terminus outside. The YE1/48 gene may have two alleles among different mouse strains and may belong to a multigene family. YE1/48 is expressed at low levels on a wide range of T cells with no restriction to their differentiation stages, and on spleen B cells as well as bone marrow cells. Its expression on lymphocytes is not related to activation or proliferation. However, YE1/48 expression appears to be induced at high levels by Abelson Murine Leukemia Virus-transformation of pre-B cells. Moreover, the epitopes defined by the YE1/48.10.6 and YE1.32.8.5 antibodies seem to be exposed only on three T lymphomas but not on normal T cells. It is thus tantalizing to speculate a correlation of the high level expression of YE1/48 antigen and its epitope exposure on transformed lymphocytes with cellular transformation. In summary, YE1/48 was found to be a novel T cell surface antigen which has similar dimeric structure as the murine T cell receptor α/β and human CD28 (T44). It has now been characterized biochemically, molecularly cloned, and its expression on lymphoid cells has been determined. Although the function of YE1/48 antigen remains unknown, a number of intriguing characteristics observed in the current studies have certainly called for further studies on the antigen and the determination of its function.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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9

Rovis, Flavia. "Functional and molecular characterisation of murine CD4+CD25+ regulatory T cells." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486557.

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CD4+CD2S+ regulatory T cells (Tregs) are naturally occurring lymphocytes that play a central role in tolerance, autoimmune diseases, transplantation, tumour immunology and infectious diseases. Despite the numerous studies carried on this' subpopulation of Tregs, the mechanisms of action of these cells still remain elusive. This project is focused on the functional and molecular characterisation .of murine Tregs with the hypotheses that they mediate suppression by contact-dependent inhibitory signal. A sensitive assay of Treg function in vitro was developed, based on the co-culture of CD2S+ and CD2S- CD4+ T cells with anti-CD3/CD28-coated DynaBeads�®. Potent, titratable suppression of both proliferation and a range of cytokines in culture supernatants - including IL-2, IL-4, IL-S, IFNy and 1NFa. - was demonstrated. This assay has subsequently been used to measure in vitro Treg function using a complex mathematical model - dev~loped in-house - showing that CD4+CD2S+ Tregs restrain the size of a co-cultured CD4+CD2S- T cell population by the simultaneous suppression of cell division and induction of cell death, mediated by both the intrinsic and extrinsic pathways. of apoptosis, using dilution of CFSE as a read-out. These studies have been complemented by the proteomic examination of freshly isolated and anti-CD3/CD28 Dynabead@-activated CD2S+ and CD2S- CD4+ T cells. A number of complex proteomic techniques have been mastered, such as liquid IEF in the first dimension, which were novel in the context of Tregs biology. In addition, new differentially expressed proteins in Tregs were discovered. In particular, a protein, 14.3.3 that may play a hitherto unrecognised role in Treg function, was identified. Overall, these studies suggest several new perspectives on Treg biology and new paths of exploration.
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Ciurkiewicz, Małgorzata [Verfasser]. "Role of regulatory T cells, cytotoxic T cells and interleukin-10 in Theiler's murine encephalomyelitis virus infection / Małgorzata Ciurkiewicz." Hannover : Stiftung Tierärztliche Hochschule Hannover, 2019. http://d-nb.info/1193489407/34.

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Books on the topic "Murine T Cells"

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Horowitz, Jay Bruce. Autocrine growth regulation of a cloned murine T helper cell line. [New Haven: s.n.], 1987.

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Geus, Bernard de. Differentiation and characterization of murine intestinal intraepithelial lymphocytes. s-Gravenhage: Pasmans Offsetdrukkerij BV, 1992.

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Tomkins, Paul Thomas. Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells. [s.l.]: typescript, 1989.

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Mammoliti, Diane. T cell cytotoxicity to acetaldehyde-modified splenocytes in the murine system. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1991.

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Identification and characterization of murine TCR [gamma] [delta]-expressing peripheral T cells. 1990.

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Tuetken, Rebecca S. Characterization of murine culture-induced cells which suppress cytolytic T lymphocyte responses. 1989.

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Koh, Dow-Rhoon. The role of CD4+, CD8+ and CD4-8-T cells in murine experimental allergic encephalomyelitis and lupus. 1993.

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Cheung, Evelyn Joyce. Characterization of the CD8 T cell response to murine gammaherpesvirus 68 infection. 2012.

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Haas, David Gerard. Cytotoxic T lymphocyte and natural killer cell responses following chemoimmunotherapy of murine L1210 leukemia. 1986.

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Book chapters on the topic "Murine T Cells"

1

Lee, James, Michel Sadelain, and Renier Brentjens. "Retroviral Transduction of Murine Primary T Lymphocytes." In Genetic Modification of Hematopoietic Stem Cells, 83–96. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-409-4_7.

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Mann, R., E. Dudley, Y. Sano, Rebeeca O’Brien, W. Born, Ch Janeway, and A. Hayday. "Modulation of Murine Self Antigens by Mycobacterial Components." In Function and Specificity of γ/δ T Cells, 151–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76492-9_20.

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Bluestone, J. A., R. Q. Cron, B. Rellahan, and L. A. Matis. "Ligand Specificity and Repertoire Development of Murine TCRγδ Cells." In Function and Specificity of γ/δ T Cells, 133–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76492-9_18.

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Chen, Xiaoniao, Fengyang Lei, Liqiang Wang, Xiaofang Xiong, and Jianxun Song. "In Vitro Differentiation of T Cells from Murine Pluripotent Stem Cells." In Methods in Molecular Biology, 131–41. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9728-2_14.

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Kaiserlian, D., K. Vidal, M. Blanc, and J. P. Revillard. "Murine gut epithelial cells present antigen to specific T cell hybridoma." In Advances in Mucosal Immunology, 38–39. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_6.

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Loos, Pauline, Lauralie Short, Gillian Savage, and Laura Evgin. "Expansion and Retroviral Transduction of Primary Murine T Cells for CAR T-Cell Therapy." In Methods in Molecular Biology, 41–53. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3593-3_4.

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Verschueren, Hendrik, Georges K. De Bruyne, Daniel Dekegel, Marc M. Mareel, and Patrick De Baetselier. "The Invasive Behaviour of Murine T-Lymphoma Cells In Vitro." In Biomechanics of Active Movement and Deformation of Cells, 455–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83631-2_17.

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Barber, Amorette. "Generation of Murine Chimeric Antigen Receptor T Cells for Adoptive T Cell Therapy for Melanoma." In Methods in Molecular Biology, 645–54. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1205-7_44.

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Allison, James P., David M. Asarnow, Mark Bonyhadi, Amy Carbone, Wendy L. Havran, Diphankar Nandi, and Janelle Noble. "γδ T Cells in Murine Epithelia: Origin, Repertoire, and Function." In Mechanisms of Lymphocyte Activation and Immune Regulation III, 63–69. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5943-2_8.

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Borst, J., Thea M. Vroom, J. D. Bos, and J. J. M. Van Dongen. "Tissue Distribution and Repertoire Selection of Human γδT Cells: Comparison With the Murine System." In Function and Specificity of γ/δ T Cells, 41–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76492-9_7.

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Conference papers on the topic "Murine T Cells"

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Leibowitz, Michael S., Nicholas S. Olimpo, Liqing Wang, Aparna Jorapur, Deepa Pookot, Maria Liousia, Evguenia Arguiri, et al. "Abstract 1585: T-regulatory cells impair CAR T cell-mediated antitumor activity in a murine solid tumor model." In 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.am2021-1585.

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Xu, Wei, Qin Lan, Hui Chen, Bing Xu, Wen Ming Zhang, Song-Guo Zheng, and Wei Shi. "Adoptive Transfer Of Induced-regulatory T Cells Effectively Attenuates Murine Airway Allergic Inflammation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4305.

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Ma, Chi, Miaojun Han, Masaki Terabe, Jay Berzofsky, Dean Felsher, and Tim Greten. "Abstract B44: The role of CD4 T cells in murine model of NASH-promoted HCC." 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-b44.

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Ma, Chi, Dean Felsher, and Tim Greten. "Abstract 3166: The role of CD4 T cells in murine model of NASH-promoted HCC." 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.am2015-3166.

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Mok, M. Y., K. Law, W. Y. Kong, Y. Lo, E. Ng, C. Luo, F. Huang, G. Chan, and K. Chan. "SAT0005 Interleukin-33 ameliorates murine lupus via induction of regulatory t cells and m2 macrophage polarisation." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7604.

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Peron, JS, A. Ligeiro de Oliveira, BA Golega, C. Soares, RM Oliveira-Filho, LV Rizzo, and W. Tavares de Lima. "Role of Female Sex Hormones over CD4+Foxp3+T Regulatory Cells in Murine Model of Asthma." 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.a3730.

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Arima, M., J. Ikari, and T. Tokuhisa. "A Role of the PHD Finger Protein 11 (Phf11) In Functions of Murine T Helper Cells." 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.a4299.

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Ito, Fumito, Noemi Fusaki, and Hidehito Saito. "Abstract 5011: generation of rejuvenated murine antigen-specific T cells by reprogramming to pluripotency and redifferentiation." 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.am2015-5011.

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Mutlu, S., K. Fytianos, C. Ferrié, C. Wotzkow, S. Steiner, A. Tschirren, A. Gazdhar, and F. Blank. "Adoptive transfer of hepatocyte growth factor transfected T cells in a bleomycin injured murine lung model." In ERS Lung Science Conference 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.lsc-2021.8.

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Torres, Ana, Amanda Shea, Wonjong Jin, Caroline Kerr, Kaleb Schroeder, Paul Clark, and Zachary Morris. "1051 Radiation dose-related temporal changes in STING-associated immune genes in murine CD8 T cells." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1051.

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Reports on the topic "Murine T Cells"

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

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The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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Hurwitz, Arthur A. Modulation of T Cell Tolerance in a Murine Model for Immunotherapy of Prostatic Adenocarcinoma. Addendum. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada475839.

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