Relevant bibliographies by topics / T-cell activation antigens

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

Academic literature on the topic 'T-cell activation antigens'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "T-cell activation antigens"

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Williams, John M., Vicki E. Kelley, Robert L. Kirkman, Nicholas L. Tilney, Michael E. Shapiro, John R. Murphy, and Terry B. Strom. "T Cell Activation Antigens: Therapeutic Implications." Immunological Investigations 16, no. 8 (January 1987): 687–723. http://dx.doi.org/10.3109/08820138709087109.

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Moody, D. B. "T Cell Activation by Lipopeptide Antigens." Science 303, no. 5657 (January 23, 2004): 527–31. http://dx.doi.org/10.1126/science.1089353.

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Rhijn, Ildiko Van, Dirk M. Zajonc, Ian A. Wilson, and D. Branch Moody. "T-cell activation by lipopeptide antigens." Current Opinion in Immunology 17, no. 3 (June 2005): 222–29. http://dx.doi.org/10.1016/j.coi.2005.04.006.

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Dallman, M. J. "Antibodies to T cell activation antigens." Immunology Letters 29, no. 1-2 (July 1991): 173. http://dx.doi.org/10.1016/0165-2478(91)90225-y.

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Qin, Yingyu, Sejin Oh, Sojung Lim, Jung Hoon Shin, Min Sang Yoon, and Se-Ho Park. "Invariant NKT cells facilitate cytotoxic T-cell activation via direct recognition of CD1d on T cells." Experimental & Molecular Medicine 51, no. 10 (October 2019): 1–9. http://dx.doi.org/10.1038/s12276-019-0329-9.

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Abstract Invariant natural killer T (iNKT) cells are a major subset of NKT cells that recognize foreign and endogenous lipid antigens presented by CD1d. Although iNKT cells are characteristically autoreactive to self-antigens, the role of iNKT cells in the regulation of cytotoxic T lymphocytes (CTL) has been elucidated using α-galactosylceramide (α-GalCer), a strong synthetic glycolipid that is presented by professional antigen presenting cells (APCs), such as dendritic cells. Despite the well-known effects of α-GalCer and dendritic cells on lipid antigen presentation, the physiological role of endogenous antigens presented by CTLs during crosstalk with iNKT cells has not yet been addressed. In this study, we found that antigen-primed CTLs with transient CD1d upregulation could present lipid self-antigens to activate the iNKT cell production of IFN-γ. CTL-mediated iNKT cell activation in turn enhanced IFN-γ production and the proliferation and cytotoxicity of CTLs. We also found that the direct interaction of iNKT cells and CTLs enhanced the antitumor immune responses of CTLs. This partially explains the functional role of iNKT cells in CTL-mediated antitumor immunity. Our findings suggest that in the absence of exogenous iNKT cell ligands, iNKT cells enhanced the CTL production of IFN-γ and CTL proliferation and cytotoxicity via direct interaction with CD1d expressed on T cells without interacting with APCs.
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Welsh, Michael D., Hilary E. Kennedy, Allister J. Smyth, R. Martyn Girvin, Peter Andersen, and John M. Pollock. "Responses of Bovine WC1+ γδ T Cells to Protein and Nonprotein Antigens of Mycobacterium bovis." Infection and Immunity 70, no. 11 (November 2002): 6114–20. http://dx.doi.org/10.1128/iai.70.11.6114-6120.2002.

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ABSTRACT WC1+ γδ T cells of Mycobacterium bovis-infected cattle are highly responsive to M. bovis sonic extract (MBSE). In mycobacterial infections of other species, γδ T cells have been shown to respond to protein and nonprotein antigens, but the bovine WC1+ γδ T-cell antigenic targets within MBSE require further definition in terms of the dominance of protein versus nonprotein components. The present study sought to characterize the WC1+ γδ T-cell antigenic targets, together with the role of interleukin-2 (IL-2), in the context of M. bovis infection. This was achieved by testing crude and defined antigens to assess protein versus nonprotein recognition by WC1+ γδ T cells in comparison with CD4+ αβ T cells. Both cell types proliferated strongly in response to MBSE, with CD4+ T cells being the major producers of gamma interferon (IFN-γ). However, enzymatic digestion of the protein in MBSE removed its ability to stimulate CD4+ T-cell responses, whereas some WC1+ γδ T-cell proliferation remained. The most antigenic protein inducing proliferation and IFN-γ secretion in WC1+ γδ T-cell cultures was found to be ESAT-6, which is a potential novel diagnostic reagent and vaccine candidate. In addition, WC1+ γδ T-cell proliferation was observed in response to stimulation with prenyl pyrophosphate antigens (isopentenyl pyrophosphate and monomethyl phosphate). High levels of cellular activation (CD25 expression) resulted from MBSE stimulation of WC1+ γδ T cells from infected animals. A similar degree of activation was induced by IL-2 alone, but for WC1+ γδ T-cell division IL-2 was found to act only as a costimulatory signal, enhancing antigen-driven responses. Overall, the data indicate that protein antigens are important stimulators of WC1+ γδ T-cell proliferation and IFN-γ secretion in M. bovis infection, with nonprotein antigens inducing significant proliferation. These findings have important implications for diagnostic and vaccine development.
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Kambayashi, Taku, Jan D. Baranski, Rebecca G. Baker, Tao Zou, Eric J. Allenspach, Jonathan E. Shoag, Peter L. Jones, and Gary A. Koretzky. "Indirect involvement of allergen-captured mast cells in antigen presentation." Blood 111, no. 3 (February 1, 2008): 1489–96. http://dx.doi.org/10.1182/blood-2007-07-102111.

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Abstract It is generally thought that mast cells influence T-cell activation nonspecifically through the release of inflammatory mediators. In this report, we provide evidence that mast cells may also affect antigen-specific T-cell responses by internalizing immunoglobulin E–bound antigens for presentation to antigen-specific T cells. Surprisingly, T-cell activation did not require that mast cells express major histocompatibility complex class II, indicating that mast cells were not involved in the direct presentation of the internalized antigens. Rather, the antigen captured by mast cells is presented by other major histocompatibility complex class II+ antigen-presenting cells. To explore how this may occur, we investigated the fate of mast cells stimulated by antigen and found that FcϵRI crosslinking enhances mast cell apoptosis. Cell death by antigen-captured mast cells was required for efficient presentation because protection of mast cell death significantly decreased T-cell activation. These results suggest that mast cells may be involved in antigen presentation by acting as an antigen reservoir after antigen capture through specific immunoglobulin E molecules bound to their FcϵRI. This mechanism may contribute to how mast cells impact the development of T-cell responses.
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Rock, K. L., E. T. Yeh, C. F. Gramm, S. I. Haber, H. Reiser, and B. Benacerraf. "TAP, a novel T cell-activating protein involved in the stimulation of MHC-restricted T lymphocytes." Journal of Experimental Medicine 163, no. 2 (February 1, 1986): 315–33. http://dx.doi.org/10.1084/jem.163.2.315.

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Five mAbs have been generated and used to characterize TAP (T cell activating protein) a novel, functional murine T cell membrane antigen. The TAP molecule is a 12-kD protein that is synthesized by T cells. By antibody crossblocking, it appears to be closely associated with a 16-kD protein on the T cell membrane also identified with a novel mAb. These molecules are clearly distinct from the major well-characterized murine T cell antigens previously described. Antibody binding to TAP can result in the activation of MHC-restricted, antigen-specific inducer T cell hybridomas that is equivalent in magnitude to maximal antigen or lectin stimulation. This is a direct effect of soluble antibody and does not require accessory cells or other factors. The activating anti-TAP mAbs are also mitogenic for normal heterogeneous T lymphocytes in the presence of accessory cells or IL-1. In addition, these antibodies are observed to modulate specific immune stimulation. Thus, the activating anti-TAP mAbs synergise with antigen-specific stimulation of T cells, while a nonactivating anti-TAP mAb inhibits antigen driven activation. These observations suggest that the TAP molecule may participate in physiologic T cell activation. The possible relationship of TAP to known physiologic triggering structures, the T3-T cell receptor complex, is considered. TAP is expressed on 70% of peripheral T cells and therefore defines a major T cell subset, making it perhaps the first example of a murine subset-specific activating protein.
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McCloskey, Megan L., Maria A. Curotto de Lafaille, Michael C. Carroll, and Adrian Erlebacher. "Acquisition and presentation of follicular dendritic cell–bound antigen by lymph node–resident dendritic cells." Journal of Experimental Medicine 208, no. 1 (December 20, 2010): 135–48. http://dx.doi.org/10.1084/jem.20100354.

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Follicular dendritic cells (DCs [FDCs]) are prominent stromal cell constituents of B cell follicles with the remarkable ability to retain complement-fixed antigens on their cell surface for extended periods of time. These retained immune complexes have long been known to provide the antigenic stimulus that drives antibody affinity maturation, but their role in cellular immunity has remained unclear. In this study, we show that FDC-retained antigens are continually sampled by lymph node–resident DCs for presentation to CD8 T cells. This novel pathway of antigen acquisition was detectable when FDCs were loaded with purified antigens bound into classical antigen–antibody immune complexes, as well as after pregnancy, when they are loaded physiologically with antigens associated with the complement-fixed microparticles released from the placenta into maternal blood. In both cases, ensuing antigen presentation was profoundly tolerogenic, as it induced T cell deletion even under inflammatory conditions. These results significantly broaden the scope of FDC function and suggest new ways that the complement system and persistent antigen presentation might influence T cell activation and the maintenance of peripheral immune tolerance.
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Moris, Arnaud, Anthony Pajot, Fabien Blanchet, Florence Guivel-Benhassine, Margarita Salcedo, and Olivier Schwartz. "Dendritic cells and HIV-specific CD4+ T cells: HIV antigen presentation, T-cell activation, and viral transfer." Blood 108, no. 5 (September 1, 2006): 1643–51. http://dx.doi.org/10.1182/blood-2006-02-006361.

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Human immunodeficiency virus (HIV)-specific CD4+ lymphocytes are preferentially infected in HIV-positive individuals. To study this preferential infection, we have derived several HIV-specific (HS) CD4+ clones. We show that in dendritic cells (DCs), HIV virion capture led to major histocompatibility complex class-II (MHC-II)-restricted viral antigen presentation and to activation of HS cells. In contrast, neither cell-free virions nor infected lymphocytes activated HS cells. In DCs, the dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN/CD209), which internalizes virions, promoted MHC-II presentation of HIV antigens. Activation of HS cells by HIV-exposed DCs triggered an efficient viral spread in lymphocytes. CD4+ clones with irrelevant antigenic specificities were not activated by HIV-exposed DCs and poorly supported viral replication under this setting. Our results unravel the mechanisms of MHC-II-restricted HIV antigen presentation by DCs and describe how HIV gains access to the very cells designed by the immune system to counteract this pathogen.
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Dissertations / Theses on the topic "T-cell activation antigens"

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Evans, Dean E. "CD40 Sustains T Cell Activation During Cognate Communication with Resting B Cells: a Dissertation." eScholarship@UMMS, 1998. http://escholarship.umassmed.edu/gsbs_diss/178.

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T and B-lymphocytes play an important role in an adaptive immune response. Communication between these two cells may result in either a humoral immune response or tolerance. Communication between T and B-lymphocytes involves a number of inducible cell surface molecules on both T and B-lymphocytes. It was the aim of this project to gain a greater understanding of the role of CD40 in the dynamic communication that occurs between naïve T-lymphocytes and resting B-lymphocytes during cognate communication. Because in vivo antigen specific T-lymphocytes are at low frequency, it is difficult to examine antigen-specific naïve T-lymphocytes. Thus, an in vitro system employing naïve antigen-specific T cell receptor (TCR) transgenic T cells and small resting B-lymphocytes that did not express CD40 was devised to examine the role of CD40 in cognate communication between naïve T-lymphocytes and resting B-lymphocytes. Upon recognition of antigen on resting B-lymphocytes that expressed CD40, T-lymphocytes proliferated, expressed the activation antigens CD69 and CD25, and remained responsive to subsequent antigen challenge. In the absence of CD40, resting B-lymphocytes did not induce sustained proliferation or sustained expression of the activation markers CD69 and CD25 on naïve T-lymphocytes, and their recovery was decreased compared to naïve T-lymphocytes that recognized antigen on resting B-lymphocytes that expressed CD40. Naïve T-lymphocytes, however, remained responsive to subsequent antigen challenge after recognition of antigen on resting CD40-/- B-lymphocytes. Recognition of antigen on resting CD40-/- B-lymphocytes also resulted in increased recovery and antigen responsiveness of T-lymphocytes when compared to controls without antigen, The role of CD40 in sustaining activation of naïve T-lymphocytes may be unique to resting B-lymphocytes, since proliferation of naïve T-lymphocytes in response to dendritic cells that did not express CD40 was similar to proliferation of naïve T-lymphocytes in response to dendritic cells that expressed CD40. The mechanism by which CD40 sustained activation of naïve T-lymphocytes was investigated by examining the induction of various costimulatory molecules on resting CD40+/- and CD40-/- B-lymphocytes during cognate interaction with naive T-lymphocytes. Induction of B7-1, upregulation of CD44 and ICAM-1, and sustained but not initial induction of B7-2 required that CD40 be expressed on resting B-lymphocytes. Expression of B7-1 and CD44H was not required for proliferation of naïve T-lymphocytes in response to antigen presented on resting B-lymphocytes. However, sustained expression of B7-2 was crucial for proliferation of naïve T-lymphocytes in response to antigen presented on resting B-lymphocytes.
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Page, Theresa Helen. "Studies of rat cell surface activation antigens : molecular characterisation of the alpha and beta chains of the interleukin-2 receptor." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280535.

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DiSanto, James Philip. "Molecular events in human T cell activation : CD4, CD8 and the human Lyt-3 molecules /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=745024391&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Honey, Karen J. "Mechanisms of transplantation tolerance." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301519.

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Jellison, Evan Robert. "CD4 T Cell-Mediated Lysis and Polyclonal Activation of B Cells During Lymphocytic Choriomeningitis Virus Infection: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/349.

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CD4 T cells and B cells are cells associated with the adaptive immune system. The adaptive immune system is designed to mount a rapid antigen-specific response to pathogens by way of clonal expansions of T and B cells bearing discrete antigen-specific receptors. During viral infection, interactions between CD4 T cells and B cells occur in a dynamic process, where B cells that bind to the virus internalize and degrade virus particles. The B cells then present viral antigens to virus-specific CD4 T cells that activate the B cells and cause them to proliferate and differentiate into virus-specific antibody-secreting cells. Yet, non-specific hypergammaglobulinemia and the production of self-reactive antibodies occur during many viral infections, and studies have suggested that viral antigen-presenting B cells may become polyclonally activated by CD4 T cells in vivo in the absence of viral engagement of the B cell receptor. This presumed polyclonal B cell activation associated with virus infection is of great medical interest because it may be involved in the initiation of autoimmunity or contribute to the long-term maintenance of B cell memory. In order to directly examine the interactions that occur between T cells and B cells, I asked what would happen to a polyclonal population of B cells that are presenting viral antigens, if they were transferred into virus-infected hosts. I performed these studies in mice using the well-characterized lymphocytic choriomeningitis virus (LCMV) model of infection. I found that the transferred population of antigen-presenting B cells had two fates. Some antigen-expressing B cells were killed in vivo by CD4 T cells in the first day after transfer into LCMV-infected hosts. However, B cells that survived the cytotoxicity underwent a dynamic polyclonal activation manifested by proliferation, changes in phenotype, and antibody production. The specific elimination of antigen-presenting B cells following adoptive transfer into LCMV-infected hosts is the first evidence that MHC class II-restricted killing can occur in vivo during viral infection. This killing was specific, because only cells expressing specific viral peptides were eliminated, and they were only eliminated in LCMV-infected mice. In addition to peptide specificity, killing was restricted to MHC class II high cells that expressed the B cell markers B220 and CD19. Mice depleted of CD4 T cells prior to adoptive transfer did not eliminate virus-specific targets, suggesting that CD4 T cells are required for this killing. I found that CD4 T cell-dependent cytotoxicity cannot be solely explained by one mechanism, but Fas-FasL interactions and perforin are mechanisms used to induce lysis. Polyclonal B cell activation, hypothesized to be the cause of virus-induced hypergammaglobulinemia, has never been formally described in vivo. Based on previous studies of virus-induced hypergammaglobulinemia, which showed that CD4 T cells were required and that hypergammaglobulinemia was more likely to occur when virus grows to high titer in vivo, it was proposed that the B cells responsible for hypergammaglobulinemia may be expressing viral antigens to virus-specific CD4 T cells in vivo. CD4 T cells would then activate the B cells. However, because the antibodies produced during hypergammaglobulinemia are predominantly not virus-specific, nonvirus-specific B cells must be presenting viral antigens in vivo. In my studies, the adoptively transferred B cells that survived the MHC class II-restricted cytotoxicity became polyclonally activated in LCMV-infected mice. Most of the surviving naïve B cells presenting class II MHC peptides underwent an extensive differentiation process involving both proliferation and secretion of antibodies. Both events required CD4 cells and CD40/CD40L interactions to occur but B cell division did not require MyD88-dependent signaling, type I interferon signaling, or interferon γ signaling within B cells. No division or activation of B cells was detected at all in virus-infected hosts in the absence of cognate CD4 T cells and class II antigen. B cells taken from immunologically tolerant donor LCMV carrier mice with high LCMV antigen load became activated following adoptive transfer into LCMV-infected hosts, suggesting that B cells can present sufficient antigen for this process during a viral infection. A transgenic population of B cells presenting viral antigens was also stimulated to undergo polyclonal activation in LCMV-infected mice. Due to the high proportion of B cells stimulated by virus infection and the fact that transgenic B cells can be activated in this manner, I conclude that virus-induced polyclonal B cell activation is independent of B cell receptor specificity. This approach, therefore, formally demonstrates and quantifies a virus-induced polyclonal proliferation and differentiation of B cells which can occur in a B cell receptor-independent manner. By examining the fate of antigen-presenting B cells following adoptive transfer into LCMV-infected mice, I have been able to observe dynamic interactions between virus-specific CD4 T cells and B cells during viral infection. Adoptive transfer of antigen-presenting B cells results in CD4 T cell-mediated killing and polyclonal activation of B cells during LCMV infection. Studies showing requirements for CD4 T cells or MHC class II to control viral infections must now take MHC class II-restricted cytotoxicity into account. Polyclonal B cell activation after viral infection has the potential to enhance the maintenance of B cell memory or lead to the onset of autoimmune disease.
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Shaulov, Angela. "The roles of inflammation and antigen in CD8 T cell expansion and memory differentiation /." Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/8328.

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Li, Cheng-Rui Michael. "The Role of Tec Kinases in CD4+ T Cell Activation: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/3.

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The Tec family tyrosine kinases Itk, Tec and Rlk are expressed in T cells. Previous studies have established that these kinases are critical for TCR signaling, leading to the activation of PLCγ1. To further understand the functions of Tec kinases in T cell activation, we took three different approaches. First, we performed a thorough analysis of CD28-mediated signaling events and functional responses with purified naïve T cells from Itk-/- mice and a highly controlled stimulation system. Data from this set of studies definitively demonstrate that CD28 costimulation functions efficiently in naïve CD4+ T cells in the absence of Itk. Second, in order to further study the functions of Tec kinases in vivo, we generated transgenic mouse lines expressing a kinase-dead (KD) mutant of Tec on the Itk-/-Rlk-/- background, hoping to study mice that are functionally deficient for all three Tec kinases. The results hint the importance of the Tec kinases in T cell development and/or survival. Finally, in order to identify potential transcriptional targets of Itk, we used microarray technology to compare global gene expression profiles of naïve and stimulated Itk-/- versus Itk+/- CD4+ T cells. This analysis provided a short list of differentially expressed genes in Itk-/- versus Itk+/- CD4 T cells, providing a starting point for further studies of Itk in T cell activation. Collectively, these studies clarified the role of Itk in CD28 signaling, revealed some unexpected aspects of Tec family kinases in T cells, and indicated potential targets of Itk-dependent signaling pathways in T cells.
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Delli, Joe. "Coreceptor and costimulatory signals organize proteins within the immunological synapse and augment proximal T cell signaling events /." Connect to full text via ProQuest. IP filtered, 2006.

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Thesis (Ph.D. in Immunology) -- University of Colorado, 2006.
Typescript. Includes bibliographical references (leaves 277-285). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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Forsgren, Stina. "Mechanisms of lymphocyte selection in physiology and autoimmune pathology." Doctoral thesis, Umeå universitet, Molekylärbiologi (Teknat- och Medfak), 1991. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-100593.

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Hernandez, Maria Genevieve H. "The Role of CD40 in Naïve and Memory CD8+ T Cell Responses: a Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/346.

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Stimulation of CD40 on APCs through CD40L expressed on helper CD4+ T cells activates and “licenses” the APCs to prime CD8+ T cell responses. While other stimuli, such as TLR agonists, can also activate APCs, it is unclear to what extent they can replace the signals provided by CD40-CD40L interactions. In this study, we used an adoptive transfer system to re-examine the role of CD40 in the priming of naïve CD8+ T cells. We find an approximately 50% reduction in expansion and cytokine production of TCR-transgenic T cells in the absence of CD40 on all APCs, and on dendritic cells in particular. Moreover, CD40-deficient and CD40L-deficient mice fail to develop endogenous CTL responses after immunization and are not protected from a tumor challenge. Surprisingly, the role for CD40 and CD40L are observed even in the absence of CD4+ T cells; in this situation, the CD8+T cell itself provides CD40L. Furthermore, we show that although TLR stimulation improves T cell responses, it cannot fully substitute for CD40. We also investigated whether CD40-CD40L interactions are involved in the generation, maintenance, and function of memory CD8+ T cells. Using a virus infection system as well as a dendritic cell immunization system, we show that the presence of CD40 on DCs and other host APCs influences the survival of activated effector cells and directly affects the number of memory CD8+ T cells that are formed. In addition, memory CD8+ T cell persistence is slightly impaired in the absence of CD40. However, CD40 is not required for reactivation of memory CD8+ T cells. It seems that CD40 signals during priming also contribute to memory CD8+ T cell programming but this function can be independent of CD4+T cells, similar to what we showed for primary responses. Altogether, these results reveal a direct and unique role for CD40L on CD8+ T cells interacting with CD40 on APCs that affects the magnitude and quality of primary as well as memory CD8+ T cell responses.
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Books on the topic "T-cell activation antigens"

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Moody, D. Branch, ed. T Cell Activation by CD1 and Lipid Antigens. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-69511-0.

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Miami Bio/Technology Winter Symposium (1990 Miami, Fla.). Advances in gene technology: The molecular biology of immune diseases and the immune reponse : proceedings of the 1990 Miami Bio/Technology Winter Symposia. Oxford: IRL Press, 1990.

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Various and Branch D. Moody. T Cell Activation by CD1 and Lipid Antigens. Springer, 2010.

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Branch, Moody D., ed. T cell activation by CD1 and lipid antigens. Berlin: Springer, 2007.

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Moody, Branch D. T Cell Activation by Cd1 and Lipid Antigens. Springer, 2008.

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T Cell Activation by CD1 and Lipid Antigens (Current Topics in Microbiology and Immunology Book 314). Springer, 2007.

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Charles, Snow E., ed. T-cell dependent and independent B-cell activation. Boca Raton: CRC Press, 1991.

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Dörner, Thomas, and Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.

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B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.
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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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van der Vlag, Johan, and Jo H. M. Berden. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.
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Book chapters on the topic "T-cell activation antigens"

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Ottenhoff, Tom, and René de Vries. "MHC Class II Ir/Is Gene Controlled Antigen Specific T Cell Activation and Disease Susceptibility: Leprosy, a Human Model." In Recognition of M. leprae antigens, 12–51. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3327-9_2.

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Williams, A. F., and A. D. Beyers. "From Marker Antigens for T Lymphocyte Subsets to Molecules that Regulate Cell Activation." In Progress in Immunology, 131–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_18.

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Olive, D., P. Dubreuil, D. Charmot, C. Mawas, and P. Mannoni. "T Cell Activation Antigens: Kinetics, Tissue Distribution, Molecular Weights, and Functions; Induction on Non T Cell Lines by Lymphokines." In Immune Regulation, 39–50. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4996-2_4.

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Del Vecchio, Luigi, Mario De Felice, Maria Caterina Turco, Michele Maio, Emilio Pace, Catia Lo Pardo, Clemente Vacca, Salvatore Venuta, and Serafino Zappacosta. "T-Activation Antigens: Kinetics of Appearance and Effect on Cell Proliferation Studied with Monoclonal Antibodies." In Leukocyte Typing II, 453–61. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4613-8587-5_37.

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Morishima, Yasuo, Tomoko Noumi, Ken-ichi Ohya, Saburo Mimami, Masao Okumura, Shin-ichi Mizuno, Ryuzo Ohno, and Kanji Miyamoto. "The Diversity of T Cell Activation Antigens. Serological Analysis Including Their Expression on Non-T Acute Lymphoblastic Leukemia Cells and B Cell Lines Derived from Adult T Cell Leukemia Patients." In Leukocyte Typing II, 351–60. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4613-8587-5_28.

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Fotedar, Arun, Michel Boyer, Wallace Smart, and Bhagirath Singh. "Antigen-Specific T-Cell Activation." In Investigation and Exploitation of Antibody Combining Sites, 283–86. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5006-4_34.

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Denegri, Jorge F., and Jeanne Peterson. "VG01 T Cell Activation Antigen Selects for Antigen Reactive Cells." In Immunobiology of HLA, 563–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_244.

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Pang, Yi-Geng, and Chien-Chung Chang. "Artificial Antigen Presentosomes for T Cell Activation." In Methods in Molecular Biology, 141–51. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0266-9_12.

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Manger, Bernard, John Imboden, and Arthur Weiss. "Role of the T3/T-Cell Antigen Receptor Complex in T-Cell Activation." In The T-Cell Receptors, 133–49. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5406-2_7.

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Cooper, Kevin D., May-Sen Lee, Darius Mehregen, Erik Hansen, Ole Baadsgaard, Steen Lisby, Gunhild Lange Vejlsgaard, et al. "Activation of Reactive Versus Malignant T Cells in Cutaneous T Cell Lymphoma: Role of Abnormal Antigen Presenting Cells and T Cell Activating Molecules." In Basic Mechanisms of Physiologic and Aberrant Lymphoproliferation in the Skin, 29–38. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1861-7_3.

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Conference papers on the topic "T-cell activation antigens"

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Byrd, Tiara, Kristen Fousek, Zakaria Grada, Kevin Aviles-Padilla, Kevin Bielamowicz, Stephen Gottschalk, Bradley S. Croix, Bradley Fletcher, Meenakshi Hegde, and Nabil Ahmed. "Abstract LB-264: Two is better than one: Adoptive T cell therapy targeting tumor antigens and the tumor endothelium potentiates T cell activation and cytolytic activity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-264.

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Rickles, F. R., W. W. Hancock, K. Kobzik, N. Hogg, and C. O’Hara. "THE DISTRIBUTION OF CROSS-LINKED FIBRIN IN HUMAN LUNG CARCINOMA PARALLELS THAT OF ACTIVATED HOST MONONUCLEAR LEUKOCYTES: IMMUNO-HISTOLOGIC STUDIES WITH MONOCLONAL ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643669.

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Previous immunohistologic studies of human lung carcinoma, using polyclonal antibodies to antigens shared between fibrinogen (FGN) and fibrin (FB), showed that FGN/FB were associated withtumor cells. These findings were interpreted as evidence of the presence of tumor-associated procoagulant activity(PCA). Wecompared the distribution of coagulation-associated proteins in 16 casesof human carcinoma of the lungofvarying histologic types, using polyclonal antibodies to FGN/FB and monoclonal antibodies (mAb) to cross-linked fibrin (XL-FB;UC-45), fibronectin (FN;PHM13), factor VIII (vWF:Ag)and a tissue factor-related antigen(TF:RAg;A1 -3)- Host mononuclear leukocytes were identifiedusing various mAb toT cells and macrophages, and studied for their expression of receptorsfor interleukin-2 (IL-2R). Positive resultsare summarizedIn addition, studies of the mononuclearcells adjacent to tumors in 12/12 casesshowed the presence of tumor-associated macrophages, 10/11 showed T cells,mainly T8+, and A/5 showed corresponding expression of IL-2R, suggesting cell activation.The use of highly specific mAb showed that XL-FB is actually more selectively distributed than is found using polyclonal antisera to FGN/FB, and indeed XL-FB was largely confined to those areas adjacent to tumors which are rich in mononuclearcells. These findings suggest that fibrin deposits in human carcinomasof the lung may be due todevelopment of PCA by activated host mononuclear cells, rather than tumor cells.This lack of XL-FB on tumor cellsinspite of A1- 3 binding suggests that TF:RAg may not be available on the tumor cell surface for the activation of clotting. Further studies are neededto define the functional capacity of PCA molecules on tumor cells and tumor-associated mononuclear cells in situ.
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Jeanneaus, Ch, and Y. Sultan. "ULTRASTRUCTURAL LOCALIZATION AND CHARACTERISATION OF VON WILLEBRAND FACTOR (VWF) AND TISSUE PLASMINOGEN ACTIVATOR (t-PA) IN ENDOTHELIAL CELLS (EC) AND MEGAKARYOCYTES (MK)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642911.

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The reciproqual localization of VWF and t-PA in EC and MK was analysed in EM using immunocytochemical techniques. In parallel, PAGE electrophoresis, zymographic analysis and immuno-blotting were also performed in cell extracts using specific polyclonal and monoclonal antibodies against VWF and t-PA. By immunofluorescence, VWF showed a dense granular pattern in EC, MK and platelets, although no fluorescence was observed with specific antibodies to t-PA. In contrast, at optical level, with peroxidase or alcaline phosphatase conjugated antibodies, t-PA antigen in EC, MK and platelets appear lightly distributed in the cytoplasm. More precise localization of both antigens was studies in EM after incubation of ultrathin sections with specific colloidal gold coupled antibodies. VWF was detected by specific antibodies in storage granules : γ -granules in MK and Weibel-Palade bodies in EC only reacted with specific antibodies when the storage granules were opened by thin section ; VWF antigen was associated with the tubular structures of these granules. In EC gold or peroxidase coupled antibodies showed the presence of t-PA antigen in rough ergastoplasmic reticulum (RER) saccules and total absence of this antigen in granule structures. After thrombin stimulation, stained vesicles revealed t-PA in the cytoplasm, vesicles which rapidly disappeared after being released. In cultured MK, t-PA was detected by immunoperoxidase in perinuclear cisternae and in small vesicles near the Golgi complex, suggesting the synthesis of t-PA by MK. Concommitantly to appearance of the t-PA, fibrinolytic activity was detected. Immediatly after platelet production fibrinolytic activity disappeared probably by association with an inhibitor. MK and EC extracts after electrophoresis, immunoblotting and zymographic analysis revealed the presence of biologically active t-PA at the same position. Thus the cells have a basal level of active t-PA which can also be seen in intact cells when deposited on fibrin films. However the fibrinolytic activity of t-PA is inhibited in absence of VWF as it is the case in EC of patients with severe forms of VW disease although t-PA antigen is normally present.
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Najab, M., Ch Jeanneau, H. Serne, M. Jozefowicz, and Y. Sultan. "INTERACTION OF HUMAN ENDOTHELIAL CELLS WITH HEPARIN-LIKE POLYMERS : INSOLUBLE SULPHONATED POLYSTYRENE RESINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643094.

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It was previously demonstrated that insoluble sulphonated polystyrene resins possessed an anticoagulant heparin-like activity in the presence of plasma. The antithrombic activity is dependent on the surface density of the sulphonated groups and involves plasmatic anti T-III. This anticoagulant activity makes this material interesting for blood compatibility concerning its effect on the coagulation system. As these anticoagulant biomaterials may be used “in vivo”, their compatibility with endothelial cells (EC) is of great interest. In the present study, EC from human umbilical cord vein were cultured in 96 well plates in presence and absence of cryoprecipitate considered as the reference culture surfaces, and in wells covered with sulphonated polystyrene beads (SPB). Cell growth in this various conditions was observed and the following parameters were compared : rate of growth of EC, presence of Von Willebrand factor (VWF) by immunofluorescence, release and synthesis of EC specific antigens : VWF, tissue plasminogen activator (T-PA) and tissue plasminogen activator inhibitor (PAI). On SPB, cellular growth was found to be in a normal range but cell morphology was somewhat different. VWF antigen was identified in cells grown either on SPB or on reference wells. Non stimulated cells, incubated in serum free medium released a basic level of VWF in the supernatant. Thrombin enhanced the release of VWF from cells cultured on coated or uncoated dishes and from cells cultured on wells covered with SPB as well. In paralell, VWF in cell extracts decreased after thrombin stimulation and no difference was observed with cells cultured in presence or in absence of SPB. Without stimulation a small amount of t-PA was only observed in the supernatant 24 H samples. Thrombin stimulation induced a comparable release of t-PA from cells cultured either on SPB or reference surfaces. t-PA synthesis, measured in cell extracts did not show significant differences. In contrast, SPB inhibited the release of PAI from EC stimulated or not stimulated by thrombin. Studies are in progress to determine whether PAI is released and absorbed by SPB or absent from the cells.
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Kwiecień, Iwona, Tomasz Skirecki, Małgorzata Polubiec-Kownacka, Dariusz Dziedzic, and Joanna Domagała-Kulawik. "Cytotoxic T cell antigen 4 and the status of T cell activation in lung cancer: local vs. systemic immune response." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4863.

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Cambier, P., F. van de werf, and D. collen. "CORONARY THROMBOLYSIS IN DOGS WITH A NONGLYCOSYLATED VARIANT OF HUMAN TISSUE-TYPE PLASMINOGEN ACTIVATOR LACKING THE FINGER AND GROWTH FACTOR DOMAINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643794.

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A variant of human tissue-type plasminogen activator (t-PA-AΔFE3X), with deletion of the NH2-terminal fibronectin-like finger (F) and epidermal growth factor (E) domains, and with amino acid substitution of Gin for Asn at all known N-linked glycosylation sites was expressed in Chinese Hamster Ovary Cells and purified to homogeneity. The thrombolytic and pharmacokinetic properties of this variant were studied in a canine model with copper coil induced thrombosis of the left anterior descending coronary artery. Infusion of t PAΔFE3X at a rate of 5 pg/kg/min for 30 min in 3 dogs resulted in a plateau level in plasma of 0.66 ± 0.08 ug/ml and induced recanalization of the coronary artery within 24 ± 4 min (mean ± SEM). Bolus injections over 2 min of 0.15 mg/kg in 3 dogs resulted in peak antigen levels in plasma of 1.6 ± 0.72 μg/ml and caused reperfusion within 14 ± 6 min. Bolus injection of 0.075 mg/kg in 3 dogs gave plasma antigen levels of 0.81 + 0.20 μg/ml and induced lysis in 31 ±15 min. Further reduction of the bolus to 0.038 mg/kg yielded plasma peak levels of 0.43 ± 0.20 μg/ml but did not cause reperfusion within 3 hours. Bolus injection of 0.075 mg/kg of natural t-PA isolated from melanoma cell culture fluid (Mel-t-PA) resulted in plasma peak levels of 0.46 ± 0.09 μg/ml and caused recanalization within 3 hours in only 1 of 4 dogs. None of the injections was associated with systemic fibrinolytic activation and fibrinogen degradation. The disposition of t-PAΔ related antigen from plasma following bolus injection could be described by a sum of two exponential terms with t1/2α: 17 min and t1/2β: 100 min. No significant difference in disposition rates for the different bolus injections were observed. Corresponding values for t1/2α of Mel-t-PA are 3 min.It is concluded that the deletion mutant t-PAΔFE3X has a markedly slower disposition rate from plasma than intact t-PA, which renders it relatively more effective than natural t-PA after bolus injection.
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Broz, Miranda, Mikhail Binnewies, Bijan Boldajipour, Amanda Nelson, Joshua Pollock, David Erle, Andrea Barczak, et al. "Abstract B65: Dissecting the tumor myeloid compartment reveals rare activating antigen presenting cells, critical for T cell immunity." 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-b65.

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Mirchandani, Ananda S., Robert J. Salmond, and Foo Y. Liew. "IL-33-Induced Type 2 Innate Lymphoid Cells Impact Upon CD4 T Cell Activation In The Absence Of Antigen Stimulation." 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.a6475.

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Glas-Greenwalt, P., J. Palascak, R. Gruppo, D. Stroop, and V. Pollak. "DEFECTIVE FIBRINOLYSIS IN SICKLE CELL DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644838.

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Vasocclusive crises (VOC) cause significant morbidity and mortality in sickle cell disease (SCD). Although sickling is thought to be the predominant factor in VOC, investigators have examined the possible role of the hemostatic mechanism in the process. The data are, however, inconsistent. We studied, functionally with the fibrin plate method, the fibrinolytic system in 36 adults in the steady state and in 8 children, 7 of whom suffered from painful crises. Values in 240 normal blood donors were: tissue-type plasminogen activator activity (t-PA); 3-25 activator units/ml, corresponding to 0.04 to 0.4 ng/ml; plasminogen activator inhibitor (PA-I): 649-885 inhibitor units/ml; and α2-antiplasmin (α2-AP) : 718-970 inhibitor units/ml. In patients with sickle cell disease t-PA levels were below the normal range in 24/44. PA-I and α2-AP levels were elevated in 35/44 and 23/44 respectively. The prevalence was similar in patients in crises and quiescent. Functionally impaired t-PA was associated with either low, normal or high t-PA antigen levels measured immunologically with an ELISA technique (normal range: 3-6 ng/ml). This indicates various degrees of endothelial dysfunction, ranging from impaired synthesis to functionally defective protein to complex formation with PA-I. Fibrin has been implicated in the intravascular sludging of sickle cells. It is suggested that a defective fibrin-clearing system contributes to the syndrome of SCD.
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Kooistra, T., J. A. van den Berg, H. A. M. Tüns, G. Platenburg, D. Rijken, and E. A. van den Berg. "BUTYRATE SPECIFICALLY STIMULATES TISSUE-TYPE PLASMINOGEN ACTIVATOR SYNTHESIS IN CULTURED HUMAN ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644656.

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In a search for compounds that can enhance tissue-type plasminogen activator (t-PA) synthesis in cultured human endothelial cells we found that dibutyryl cyclic AMP (at a concentration of 2 mM) led to a several-fold increase in t-PA production by endothelial cells over a 24 h incubation period. Further researchshowed that this stimulating effectcould be explained by the slow liberation of butyrate, as the effect could be reproduced by addition of free butyrate to the medium, but notby addition of 8-bromo cyclic AMP. With butyrate, an accelerated accumulation of t-PA antigen in the conditioned medium (CM) was observed after a lag period of about 6 h. Increasing amounts of butyrate caused anincreasingly stimulatory effect, reaching a plateau with 5 mM butyrate. The relative increase in t-PAproduction in thempresence of 5 mM butyrate varied among different endothelial cell cultures from 6 to 25-fold in 24 h CM. The butyrate-induced increase in t-PA production wasaccompanied by increased t-PA mRNAlevels.Analysis of radiolabelled CM andcell extracts by SDS-PAGE and autoradiography indicated that the potent action of butyrate is restricted to a limited group of proteins. We found that theaccumulation of PA-inhibitor activity in CM from butyrate-treated cells increased only moderately.In our study of the relationshipbetween structure and stimulatory activity we found that butyrate wasby far the most effective inducer oft-PA synthesis. Shortening or lengthening the carbon chain by one carbon atom decreased the stimulatory effect after 24 h of incubation by 50-70%. Further changes in the length of the carbon chain almost completely suppressed the stimulatory activity. Similarly, alterations of the aliphatic chain by introduction of functional groups, a double bond or a branched structure rendered butyrate ineffective in increasing t-PA synthesis. Thus, a straight-chain C4 monocarboxylate structure with a methyl group at one end and a carboxyl moiety at the other seems to be required for the rather specific induction of t-PA synthesis in cultured human endothelialcells.
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