Relevant bibliographies by topics / Costimulation

Contents

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

Academic literature on the topic 'Costimulation'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Costimulation"

1

Loomis, William H., Sachiko Namiki, David B. Hoyt, and Wolfgang G. Junger. "Hypertonicity rescues T cells from suppression by trauma-induced anti-inflammatory mediators." American Journal of Physiology-Cell Physiology 281, no. 3 (September 1, 2001): C840—C848. http://dx.doi.org/10.1152/ajpcell.2001.281.3.c840.

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Trauma causes the release of anti-inflammatory factors thought to cause infections by inhibiting T cells. We have found that hypertonic saline (HS) enhances functions of normal T cells. Here we studied if HS can rescue T cells from suppression by costimulating interleukin (IL)-2 production. Human peripheral blood mononuclear cells were treated with the immunosuppressive factors IL-4, IL-10, transforming growth factor (TGF)-β1, and PGE2and with serum of trauma patients and stimulated with phytohemagglutinin, and IL-2 production was measured. Costimulation with HS tripled IL-2 production of normal cells. IL-4, IL-10, TGF-β1, and PGE2suppressed IL-2 production with IC50of 500, 1, 36,000, and 0.01 pg/ml, respectively. Costimulation of suppressed cells with HS restored IL-2 production and increased IC50values >70-fold. Serum from trauma patients could completely suppress normal cells; however, costimulation with HS restored IL-2 production by up to 80% of the control response. These findings show that HS can restore the function of suppressed T cells, suggesting that HS resuscitation of trauma patients could reduce posttraumatic sepsis.
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Kinnear, Gillian, Nick D. Jones, and Kathryn J. Wood. "Costimulation Blockade." Transplantation Journal 95, no. 4 (February 2013): 527–35. http://dx.doi.org/10.1097/tp.0b013e31826d4672.

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van der Merwe, P. Anton. "Modeling costimulation." Nature Immunology 1, no. 3 (September 2000): 194–95. http://dx.doi.org/10.1038/79729.

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Visan, Ioana. "Networks for costimulation." Nature Immunology 14, no. 9 (August 20, 2013): 892. http://dx.doi.org/10.1038/ni.2699.

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Tivol, Elizabeth A., A. Nicola Schweitzer, and Arlene H. Sharpe. "Costimulation and autoimmunity." Current Opinion in Immunology 8, no. 6 (December 1996): 822–30. http://dx.doi.org/10.1016/s0952-7915(96)80011-2.

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Kremer, Joel M. "Selective Costimulation Modulators." JCR: Journal of Clinical Rheumatology 11, Supplement (June 2005): S55—S62. http://dx.doi.org/10.1097/01.rhu.0000166626.68898.17.

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Sharpe, Arlene H. "Mechanisms of costimulation." Immunological Reviews 229, no. 1 (May 2009): 5–11. http://dx.doi.org/10.1111/j.1600-065x.2009.00784.x.

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Webb, LM, and M. Feldmann. "Critical role of CD28/B7 costimulation in the development of human Th2 cytokine-producing cells." Blood 86, no. 9 (November 1, 1995): 3479–86. http://dx.doi.org/10.1182/blood.v86.9.3479.bloodjournal8693479.

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CD28 is a major costimulatory signal receptor for T cells. We have used human naive CD4+ cells from cord blood to analyze the effect of the CD28/B7 costimulatory pathway on development of T helper (Th) subsets. We show that CD28 costimulation is critical for development of the Th2 cytokine-producing cells and that in the absence of CD28 costimulation, cells are not primed to produce Th2 cytokines and consequently “default” to the Th1 subset, independent of the presence of exogenous cytokines. After CD28 costimulation, cells differentiate into a subset that produces Th2 cytokines. However, further CD28 costimulation is not required to maintain Th2 cytokine production. We conclude that D28 costimulation is critical for the development of Th0 and Th2 subsets, but not for the maintenance of cytokine production.
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O’Dwyer, Ronan, Marina Kovaleva, Jiquan Zhang, John Steven, Emma Cummins, Deborah Luxenberg, Alfredo Darmanin-Sheehan, et al. "Anti-ICOSL New Antigen Receptor Domains Inhibit T Cell Proliferation and Reduce the Development of Inflammation in the Collagen-Induced Mouse Model of Rheumatoid Arthritis." Journal of Immunology Research 2018 (October 17, 2018): 1–13. http://dx.doi.org/10.1155/2018/4089459.

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Lymphocyte costimulation plays a central role in immunology, inflammation, and immunotherapy. The inducible T cell costimulator (ICOS) is expressed on T cells following peptide: MHC engagement with CD28 costimulation. The interaction of ICOS with its sole ligand, the inducible T cell costimulatory ligand (ICOSL; also known as B7-related protein-1), triggers a number of key activities of T cells including differentiation and cytokine production. Suppression of T cell activation can be achieved by blocking this interaction and has been shown to be an effective means of ameliorating disease in models of autoimmunity. In this study, we isolated specific anti-ICOSL new antigen receptor domains from a synthetic phage display library and demonstrated their ability to block the ICOS/ICOSL interaction and inhibit T cell proliferation. Anti-mouse ICOSL domains, considered here as surrogates for the use of anti-human ICOSL domains in patient therapy, were tested for efficacy in a collagen-induced mouse model of rheumatoid arthritis where they significantly decreased the inflammation of joints and delayed and reduced overall disease progression and severity.
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Cai, Z., and J. Sprent. "Influence of antigen dose and costimulation on the primary response of CD8+ T cells in vitro." Journal of Experimental Medicine 183, no. 5 (May 1, 1996): 2247–57. http://dx.doi.org/10.1084/jem.183.5.2247.

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The influence of costimulation on the primary response of CD8+ T cells to class I alloantigens was studied with the aid of a T cell receptor transgenic model and defined peptides as antigen. With small doses of antigen, the proliferative response of CD8+ cells was high early in culture but was of brief duration and declined to low levels by day 4; this abbreviated response was associated with limited production of interleukin 2 (IL-2) and was strongly dependent upon costimulation via CD8-major histocompatibility complex class I and CD28-B7 interactions. The response to large doses of antigen was quite different in two respects. First, large doses of antigen inhibited the early (day 3) proliferative response but caused a marked elevation of the response late in culture (day 5); these altered kinetics were associated with increased production of IL-2. Second, the initial proliferative response to large doses of antigen did not require costimulation: indeed, blocking costimulation with CTLA4lg or anti-CD8 monoclonal antibody enhanced the early proliferative response. However, blocking costimulation impaired IL-2 production and prevented the late proliferative response. These findings indicate that the requirement for costimulation of T cells can be partly overcome by increasing the dose of antigen to a high level. However, costimulation plays a key role in prolonging the response, presumably by triggering strong and sustained production of IL-2.
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Dissertations / Theses on the topic "Costimulation"

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Watson, Martin Peter. "Lymphocyte costimulation in corneal allograft rejection." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498610.

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Lute, Kenneth D. "Costimulation and tolerance in T cell immunotherapy." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141850521.

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Parra, Eduardo. "Molecular basis for costimulation of human T lymphocytes." Lund : Lund University, 1998. http://books.google.com/books?id=SgFrAAAAMAAJ.

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Suzuki-Jaecks, Ivy. "Fas ligand-mediated costimulation in peripheral T lymphocytes /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8319.

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Kumar, Gaurav. "Infections humaines et molécules de costimulation lymphocytaires T." Nice, 2012. http://www.theses.fr/2012NICE4057.

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Les maladies infectieuses, causées par divers microorganismes, sont la première cause de mort à travers le monde. Les lymphocytes T sont une population variée de cellules qui participent aux immunités innée et adaptative. Nous cherchons à caractériser les réponses lymphocytaires T lors des infections bactériennes et virales chez l’homme. Notre recherche, menée à partir de prélèvement humains, s’est portée sur l’infection osseuse (IO) bactérienne chronique, sur le Syndrome de Détresse Respiratoire Aiguë de l’adulte (SDRA), et sur l’infection par le Virus de l’Immunodéficience Humaine (VIH). Les IO sont caractérisées par une augmentation de l’activation et une diminution de la prolifération lymphocytaire T, associées à une diminution de CD28 et une augmentation de la molécule de costimulation CTLA4 au sein de la population CD4. La sous-population T CD4+CD28- a des capacités cytolitiques accrues comparativement aux lymphocytes T CD28+, avec une augmentation de la sécrétion de perforine. Au cours du SDRA, l’activation et la prolifération des lymphocytes T alvéolaires sont associées à une augmentation de l’expression de CLTA4, en lien avec la présence de clones TH-17. L’IL17 participerait à une attraction de l’expression de CTLA4, en lien avec la présence de clones TH-17. L’IL17 participerait à l’attraction des polynucléaires neutrophiles pouvant initier la fibrose observée lors d’un SDRA. Au cours du VIH, l’introduction d’un anti-intégrase en complément d’une trithérapie usuelle efficace diminue l’ADN viral intracellulaire dans les T CD4, et est associé à une augmentation de CD28 et une diminution de CTLA4 sur ces mêmes cellules, et à une inhibition relative du taux d’apoptose. En conclusion, les modifications de molécules de costimulation lymphocytaires T sont dépendantes du site d’infection et/ou du stade aigu ou chronique de l’infection, et non de l’agent pathogène en cause. Les traitements anti-infectieux peuvent modifier l’expression de ces molécules de costimulation, les thérapies ciblant ces molécules devant donc intégrer ces critères cinétiques
Infectious diseases, caused by various microorganisms are the major cause of death worldwide. T-lymphocytes are a diverse population of cells that participate in both innate and adaptive immunity. We are defining human T lymphocyte responses to viral and bacterial infection and their role on protective immunity and disease pathogenesis. Our research focuses on chronic and acute bacterial and viral infection in Osteomyelities, Acute respiratory distress syndrome (ARDS) and human Immunodeficiency virus (HIV). Our research is largely clinically based because these diseases do not have good experimental animal models. We report increased T-cell activation and decreased proliferation along with the alteration of its costimulatory pathways as hallmarks of bacterial bone infections in humans. A remarkable decrease in the CD28 expression on CD4 T cells was observed in infected bone tissues along with increased CTLA4 expression. On further analysis of CD28 negative CD4 T cell population, it seemed that it has enhanced cytotoxic capabilities in comparison to their CD28 positive counterparts, being obvious by increased perforine secretion. In ARDS we observed increased activated and proliferating T cell phenotype with increased CTLA4 expression, suggesting that increased CTLA4 seems to play a suppressive role in order to achieve normal T cell homeostasis after going through the active phase of activation. Also we observed IL-17 secretion in ARDS, which may suggest the role of IL-17 as a chemoattractant for neutrophils at the site of infection. In AIDS, the included patients had a stable HAART treatment with undetectable viral load for at least six months. In our study we did not observed major alteration in T cell phenotype and its costimulatory molecules after Raltegravir introduction, but we observed a decrease in viral load in CD4 T cells. In conclusion, alteration of the costimulatory molecules appeared to be disease-related but not pathogen specific
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Tuladhar, Rashmi. "ROLE OF COSTIMULATION IN EXPERIMENTAL LEISHMANIA MEXICANA INFECTION." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1395619402.

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Cameron, Mark J. "Cytokine- and costimulation-mediated therapy of type 1 diabetes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0021/NQ58397.pdf.

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May, Kenneth F. "T cell costimulation in anti-tumor immunity and autoimmunity." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1085004772.

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Thesis (Ph. D.)--Ohio State University, 2004.
Document formatted into pages; contains xv, 178 p. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2006 May 20.
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Briggs, Zoe Louise. "CD28 costimulation in T cells : requirements, outcomes and regulation." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5378/.

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The costimulatory receptor CD28 and its inhibitory counterpart CTLA-4 share the same ligands and comprise a crucial checkpoint in T cell activation. CTLA-4 removes its ligands from antigen presenting cells by trans-endocytosis, which reduces the availability of costimulatory ligands for CD28 engagement to regulate T cell activation. This project examined the functional implications of reducing the availability of costimulatory molecules for CD4 T cell responses, and investigated the use of trans-endocytosis by other T cell receptors. Surprisingly, it was revealed that PD-1 and OX40 can also internalise their ligands, although perhaps not via the same mechanism as CTLA-4 trans-endocytosis. It was also shown that altering the availability of CD28 ligands affects the extent of T cell proliferation, suggesting that CTLA-4 trans-endocytosis can finely tune the T cell response. Furthermore, it was observed that CD28 costimulation is not always required for T cell activation and proliferation, but CD28 engagement is required for the optimal upregulation of a number of effector proteins and for TH2 cytokine production. Interestingly, T cells activated in the absence of CD28 signalling were not classically anergic. Strikingly, it was also found that memory T cells are dependent on CD28 costimulation.
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May, Kenneth F. Jr. "T cell costimulation in anti-tumor immunity and autoimmunity." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1085004772.

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Books on the topic "Costimulation"

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Lau, Peggy. The role of 4-1BB/4-1BB ligand costimulation in T cell responses. Ottawa: National Library of Canada, 2001.

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Saoulli, Catherine. CD28-independent, TRAF2-dependent costimulation of resting T cells by 4-1BB ligand. Ottawa: National Library of Canada, 1998.

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Mir, Manzoor Ahmad. Reverse Costimulation in the Treatment of Infectious Diseases. Nova Science Publishers, Incorporated, 2014.

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Dawicki, Wojciech. The role of 4-1BB (CD 137) and OX40 (CD 134) costimulation in T cell immunity in vivo. 2005.

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Isaacs, John D., and Philip M. Brown. Rituximab and abatacept. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0083.

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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept's licence permits it use as a first-line biologic. In the United Kingdom, however, the National Institute for Health and Clinical Excellence (NICE) restricts the use of abatacept to patients who develop adverse effects with rituximab or in whom rituximab is contraindicated. As with other biologics, the use of either drug is associated with an enhanced risk of serious infections; additionally, rituximab in particular can cause infusion reactions, requiring prophylaxis. By targeting cells that are central to RA pathogenesis, these drugs provide important additional therapeutic options for patients with RA.
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Book chapters on the topic "Costimulation"

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Bloom, Roy D., and Laurence A. Turka. "Costimulation Blockade." In Current and Future Immunosuppressive Therapies Following Transplantation, 265–77. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-1005-4_15.

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Gilman, S. C., and R. J. Noelle. "Molecular mechanisms of costimulation." In Therapeutic Strategies for Modulating the Inflammatory Diseases, 15–16. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8857-8_3.

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Yeung, Melissa Y., Tanja Grimmig, and Mohamed H. Sayegh. "Costimulation Blockade in Transplantation." In Co-signal Molecules in T Cell Activation, 267–312. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9717-3_10.

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Weinberg, Andrew D., Dean E. Evans, and Arthur A. Hurwitz. "Accentuating Tumor Immunity Through Costimulation." In Cancer Immunotherapy at the Crossroads, 173–94. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-743-7_10.

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Chen, Lieping. "Overcoming T Cell Ignorance by Providing Costimulation." In Advances in Experimental Medicine and Biology, 159–65. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5357-1_26.

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Daikh, David I., and David Wofsy. "Treatment of Autoimmunity by Inhibition of T Cell Costimulation." In Advances in Experimental Medicine and Biology, 113–17. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1243-1_12.

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Bucks, Christine M., and Peter D. Katsikis*. "NEW INSIGHTS INTO CLASSICAL COSTIMULATION OF CD8+ T CELL RESPONSES." In Crossroads between Innate and Adaptive Immunity II, 91–111. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-79311-5_9.

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Azuma, M., and L. L. Lanier. "The Role of CD28 Costimulation in the Generation of Cytotoxic T Lymphocytes." In Pathways for Cytolysis, 59–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79414-8_4.

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van den Berg, Hugo A., and Andrew K. Sewell. "Dynamic Tuning of T Cell Receptor Specificity by Co-Receptors and Costimulation." In Mathematical Models and Immune Cell Biology, 47–73. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-7725-0_3.

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Pree, Ines, and Thomas Wekerle. "Inducing Mixed Chimerism and Transplantation Tolerance Through Allogeneic Bone Marrow Transplantation With Costimulation Blockade." In Immunological Tolerance, 391–403. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-395-0_25.

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Conference papers on the topic "Costimulation"

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Drozda, Martin, and Sven Schaust. "Costimulation and priming: Can it help protect ad hoc wireless networks?" In 2009 2nd International Symposium on Applied Sciences in Biomedical and Communication Technologies (ISABEL). IEEE, 2009. http://dx.doi.org/10.1109/isabel.2009.5373649.

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Schrand, Brett, Randall Brenneman, Alexey Berezhnoy, and Eli Gilboa. "Abstract A25: Targeting costimulation to the tumor stroma with bispecific oligonucleotide aptamers." 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-a25.

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Aznar, M. Angela, Sara Labiano, Angel Diaz-Lagares, Manel Esteller, Juan Sandoval, and Ignacio Melero. "Abstract 612: Methylation changes in DNA of CD8 T cells following CD137 costimulation." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-612.

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Wesselkamper, SC, GT Motz, BL Eppert, and MT Borchers. "Role of NKG2D and Toll-Like Receptor Costimulation in Activation of Natural Killer 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.a5737.

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Schreiber, Taylor H., Louis Gonzalez, Dietlinde Wolf, Maria Bodero, and Eckhard R. Podack. "Abstract A38: T cell costimulation by TNFRSF4, TNFRSF18, and TNFRSF25 in the context of vaccination." 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-a38.

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Schrand, Brett, Bhavna Verma, Agata Levay, Shradha Patel, Iris Castro, Ana Paula Benaduce, Randall Brenneman, et al. "Abstract 1700: Radiation-induced vegf-targeted 4-1bb costimulation enhances immune control of tumor growth." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1700.

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Li, Peng, Xin Du, Yun Xin, Jianyu Weng, and Peilong Lai. "Abstract 618: Toll-like receptor 2 costimulation potentiates the antitumor efficacy of CAR T cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-618.

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Schultz, Liora M., Debra Czerwinski, Chiung-Chi Kuo, Shoshana Levy, and Ronald Levy. "Abstract 2209: Costimulation of T cells by CD81 enhances CAR transduction of naive T cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2209.

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Labiano, Sara, Asís Palazón, José I. Quetglas, Elixabet Bolaños, Arantza Azpilicueta, Aizea Morales-Kastresana, Alfonso Rodriguez, et al. "Abstract 4058: Hypoxia-induced soluble CD137 in malignant cells blocks CD137L-costimulation as an immune escape mechanism." 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.am2015-4058.

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Murata, Satoshi, Tomoyuki Ueki, Naomi Kitamura, Eiji Mekata, Tomoharu Shimizu, Hisanori Shiomi, Hajime Abe, et al. "Abstract 1939: Augmenting effector function and abrogating Treg function by OX40 costimulation enhances adoptive transfer tumor-specific CTL response." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1939.

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Reports on the topic "Costimulation"

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Weinberg, Andrew D. Tumor Specific CD4+ T-Cell Costimulation Through a Novel Receptor/Ligand Interaction. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada374764.

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Weinberg, Andrew D. Tumor Specific CD4+ T-Cell Costimulation Through a Novel Receptor Ligand Interaction. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359629.

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