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Journal articles on the topic 'Costimulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Inman, Brant, Xavier Frigola, Haidong Dong, and Eugene Kwon. "Costimulation, Coinhibition and Cancer." Current Cancer Drug Targets 7, no. 1 (February 1, 2007): 15–30. http://dx.doi.org/10.2174/156800907780006878.

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12

Martin-Orozco, Natalia, and Chen Dong. "New battlefields for costimulation." Journal of Experimental Medicine 203, no. 4 (April 10, 2006): 817–20. http://dx.doi.org/10.1084/jem.20060219.

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Costimulation regulates the activation of naive T cells as they first encounter antigens in the secondary lymphoid organs. But recently characterized costimulatory molecules of the B7 family appear to have roles beyond initial T cell activation. New evidence shows that negative costimulators expressed by tumors and normal tissues afford local protection from T cell–mediated attack.

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13

Schwartz, Jean-Claude D., Xuewu Zhang, Stanley G. Nathenson, and Steven C. Almo. "Structural mechanisms of costimulation." Nature Immunology 3, no. 5 (May 2002): 427–34. http://dx.doi.org/10.1038/ni0502-427.

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14

BUGEON, LAURENCE, and MARGARET J DALLMAN. "Costimulation of T Cells." American Journal of Respiratory and Critical Care Medicine 162, supplement_3 (October 2000): S164—S168. http://dx.doi.org/10.1164/ajrccm.162.supplement_3.15tac5.

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15

Adams, Andrew B., Christian P. Larsen, and Thomas C. Pearson. "Costimulation blockade and tolerance." Current Opinion in Organ Transplantation 7, no. 1 (March 2002): 7–12. http://dx.doi.org/10.1097/00075200-200203000-00003.

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16

Paterson, Alison M., Vijay K. Vanguri, and Arlene H. Sharpe. "SnapShot: B7/CD28 Costimulation." Cell 137, no. 5 (May 2009): 974–974. http://dx.doi.org/10.1016/j.cell.2009.05.015.

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17

van Seventer, G. A., W. Newman, Y. Shimizu, T. B. Nutman, Y. Tanaka, K. J. Horgan, T. V. Gopal, E. Ennis, D. O'Sullivan, and H. Grey. "Analysis of T cell stimulation by superantigen plus major histocompatibility complex class II molecules or by CD3 monoclonal antibody: costimulation by purified adhesion ligands VCAM-1, ICAM-1, but not ELAM-1." Journal of Experimental Medicine 174, no. 4 (October 1, 1991): 901–13. http://dx.doi.org/10.1084/jem.174.4.901.

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Many ligands of adhesion molecules mediate costimulation of T cell activation. The generality of this emerging concept is best determined by using model systems which exploit physiologically relevant ligands. We developed such an "antigen-specific" model system for stimulation of resting CD4+ human T cells using the following purified ligands: (a) major histocompatibility complex class II plus the superantigen Staphylococcus enterotoxin A, to engage the T cell receptor (TCR); (b) adhesion proteins vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), and endothelial leukocyte adhesion molecule 1 (ELAM-1), to provide potential cell surface costimulatory signals; and (c) recombinant interleukin 1 beta (rIL-1 beta)/rIL-6 as costimulatory cytokines. In this biochemically defined system, we find that resting CD4+ T cells require costimulation in order to respond to TCR engagement. This costimulation can be provided by VCAM-1 or ICAM-1; however adhesion alone is not sufficient since ELAM-1 mediates adhesion but not costimulation. The cytokines IL-1 beta and IL-6 by themselves cannot mediate costimulation, but augment the adhesion ligand-mediated costimulation. Direct comparison with the model of TCR/CD3 engagement by CD3 monoclonal antibody demonstrated comparable costimulatory requirements in both systems, thereby authenticating the commonly used CD3 model. The costimulation mediated by the activation-dependent interaction of the VLA-4 and LFA-1 integrins with their respective ligands VCAM-1 and ICAM-1 leads to increased IL-2R alpha (CD25) expression and proliferation in both CD45RA+ CD4+ and CD45RO+ CD4+ T cells. The integrins also regulate the secretion of IL-2, IL-4, and granulocyte/macrophage colony-stimulating factor. In contrast the activation-independent adhesion of CD4+ T cell to ELAM-1 molecules does not lead to T cell stimulation as measured by proliferation, IL-2R alpha expression, or cytokine release. These findings imply that adhesion per se is not sufficient for costimulation, but rather that the costimulation conferred by the VLA-4/VCAM-1 and LFA-1/ICAM-1 interactions reflects specialized accessory functions of these integrin pathways. The new finding that VLA-4/VCAM-1 mediates costimulation adds significance to observations that VCAM-1 is expressed on a unique set of potential antigen-presenting cells in vivo.

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18

Kinchington, D., T. Ng, N. Mathews, M. Tisdale, D. Devine, and WO Ayuko. "T Cell Costimulation by Derivatives of Benzoic Acid." Antiviral Chemistry and Chemotherapy 8, no. 2 (April 1997): 121–30. http://dx.doi.org/10.1177/095632029700800206.

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A number of analogues of benzoic acid were evaluated in a T cell costimulation assay. One compound, the sodium salt of 2-chloro-5-nitrobenzoic acid (CNBA-Na) was chosen for further study and was found to be a potent costimulator of anti-CD3-induced proliferation of both H9 lymphoblastoid cells ( P<0.001) and human peripheral blood mononuclear cells ( P=0.001) in a dose-dependent manner. The costimulatory effect of CNBA-Na on CD3-triggered DNA synthesis did not enhance human immunodeficiency virus replication in infected cells. Studies with blocking monoclonal antibodies against B7-1 or B7-2 indicated that the immunopotentiatory effect of CNBA-Na required a macromolecular interaction between CD28 (a costimulatory receptor on T cells) and its counter receptor B7 expressed on antigen-presenting cells. The discovery that this low molecular weight compound causes T cell proliferation highlights a potentially novel therapeutic approach to immunodeficiency diseases.

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19

Thebeau, Lydia G., and Lynda A. Morrison. "B7 Costimulation Plays an Important Role in Protection from Herpes Simplex Virus Type 2-Mediated Pathology." Journal of Virology 76, no. 5 (March 1, 2002): 2563–66. http://dx.doi.org/10.1128/jvi.76.5.2563-2566.2002.

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ABSTRACT We have used mice lacking both B7-1 and B7-2 costimulation molecules (B7KO) to investigate the effects of B7 costimulation on herpes simplex virus type 2 (HSV-2) pathogenesis. B7KO mice infected intravaginally with virulent HSV-2 showed more severe genital and neurologic disease and higher mortality rates than their wild-type counterparts. These results suggest that B7 costimulation molecules play an important role in the development of primary immune responses protective against HSV-2.

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20

de Wit, Jelle, Yuri Souwer, Astrid J. van Beelen, Rosa de Groot, Femke J. M. Muller, Hanny Klaasse Bos, Tineke Jorritsma, Martien L. Kapsenberg, Esther C. de Jong, and S. Marieke van Ham. "CD5 costimulation induces stable Th17 development by promoting IL-23R expression and sustained STAT3 activation." Blood 118, no. 23 (December 1, 2011): 6107–14. http://dx.doi.org/10.1182/blood-2011-05-352682.

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Abstract IL-17–producing CD4+ T helper (Th17) cells are important for immunity against extracellular pathogens and in autoimmune diseases. The factors that drive Th17 development in human remain a matter of debate. Here we show that, compared with classic CD28 costimulation, alternative costimulation via the CD5 or CD6 lymphocyte receptors forms a superior pathway for human Th17-priming. In the presence of the Th17-promoting cytokines IL-1β, IL-6, IL-23, and transforming growth factor-β (TGF-β), CD5 costimulation induces more Th17 cells that produce higher amounts of IL-17, which is preceded by prolonged activation of signal transducer and activator of transcription 3 (STAT3), a key regulator in Th17 differentiation, and enhanced levels of the IL-17–associated transcription factor retinoid-related orphan receptor-γt (ROR-γt). Strikingly, these Th17-promoting signals critically depend on CD5-induced elevation of IL-23 receptor (IL-23R) expression. The present data favor the novel concept that alternative costimulation via CD5, rather than classic costimulation via CD28, primes naive T cells for stable Th17 development through promoting the expression of IL-23R.

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21

Parra, E., M. Varga, G. Hedlund, T. Kalland, and M. Dohlsten. "Costimulation by B7-1 and LFA-3 targets distinct nuclear factors that bind to the interleukin-2 promoter: B7-1 negatively regulates LFA-3-induced NF-AT DNA binding." Molecular and Cellular Biology 17, no. 3 (March 1997): 1314–23. http://dx.doi.org/10.1128/mcb.17.3.1314.

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We have characterized the regulation of nuclear factors involved in transcriptional control of the interleukin-2 (IL-2) promoter-enhancer activity in Jurkat T cells stimulated with superantigen presented on HLA-DR transfectants combined with the ligands LFA-3 (CD58) and B7-1 (CD80). Gel shift analyses showed that NF-AT was strongly induced in LFA-3-costimulated Jurkat T cells, suggesting that NF-AT is a key target nuclear factor for the CD2-LFA-3 pathway. Studies using HLA-DR-B7-1-LFA-3 triple transfectants showed that the LFA-3-induced NF-AT DNA binding activity was negatively regulated by B7-1 costimulation. In contrast, induction of a CD28 response complex containing only c-Rel proteins was seen after B7-1 costimulation. Both LFA-3 costimulation and B7-1 costimulation induced the AP-1 and NF-kappaB nuclear factors. Distinct compositions of the NF-AT complexes were seen in B7-1- and LFA-3-costimulated cells. LFA-3 induced primarily Jun-D, Fra-1, and Fra-2, while B7-1 induced June-D-Fos complexes. In contrast, AP-1 and NF-kappaB complexes induced in B7-1- and LFA-3-costimulated T cells showed similar contents. Transient transfection of Jurkat T cells with a construct encoding the IL-2 enhancer-promoter region (position -500 to +60) linked to a luciferase reporter gene revealed that B7-1 costimulation was required to induce strong transcriptional activity. Combined B7-1-LFA-3 costimulation resulted in a synergistic increase in IL-2 transcriptional activity. Multimers of the AP-1, NF-AT, NF-kappaB, and CD28 response elements showed distinct kinetics and activity after LFA-3 and B7-1 costimulation and revealed that B7-1 and LFA-3 converge to superinduce transcriptional activity of the AP-1, NF-AT, and CD28 response elements. Transcriptional studies with an IL-2 enhancer-promoter carrying a mutation in the CD28 response element site revealed that the activity was reduced by 80% after B7-1 and B7-1-LFA-3 costimulation whereas the transcriptional activity induced by LFA-3 was unaffected. Our data strongly suggest a selectivity in induction of nuclear factors by the CD2-LFA-3 and CD28-B7-1 pathways. This selectivity may contribute to regulation of the levels of IL-2 induced by LFA-3 and B7-1 costimulation and favor autocrine and paracrine T-cell responses, respectively.

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22

Iwai, Hideyuki, Yuko Kozono, Sachiko Hirose, Hisaya Akiba, Hideo Yagita, Ko Okumura, Hitoshi Kohsaka, Nobuyuki Miyasaka, and Miyuki Azuma. "Amelioration of Collagen-Induced Arthritis by Blockade of Inducible Costimulator-B7 Homologous Protein Costimulation." Journal of Immunology 169, no. 8 (October 15, 2002): 4332–39. http://dx.doi.org/10.4049/jimmunol.169.8.4332.

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23

Weaver, Timothy, A. "Costimulation blockade: towards clinical application." Frontiers in Bioscience 13, no. 13 (2008): 2120. http://dx.doi.org/10.2741/2829.

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24

Kohsaka, Hitoshi. "3. T-cell Costimulation Blocker." Nihon Naika Gakkai Zasshi 100, no. 10 (2011): 2979–84. http://dx.doi.org/10.2169/naika.100.2979.

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25

Liu, Y. "Costimulation of T-cell growth." Current Opinion in Immunology 4, no. 3 (June 1992): 265–70. http://dx.doi.org/10.1016/0952-7915(92)90075-p.

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26

Greenfield, Edward A., Khuong A. Nguyen, and Vijay K. Kuchroo. "CD28/B7 Costimulation: A Review." Critical Reviews™ in Immunology 18, no. 5 (1998): 389–418. http://dx.doi.org/10.1615/critrevimmunol.v18.i5.10.

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27

Dustin, Michael L., and Andrey S. Shaw. "Costimulation: Building an Immunological Synapse." Science 283, no. 5402 (January 29, 1999): 649–50. http://dx.doi.org/10.1126/science.283.5402.649.

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28

Cho, H. R., B. Kwon, J. S. Lee, and R. J. Kim. "COSTIMULATION AS A GVHD PROPHYLAXIS." Transplantation 86, Supplement (July 2008): 408. http://dx.doi.org/10.1097/01.tp.0000331557.41974.7e.

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29

Guerder, Sylvie, and Richard A. Flavell. "Costimulation in Tolerance and Autoimmunity." International Reviews of Immunology 13, no. 2 (January 1995): 135–46. http://dx.doi.org/10.3109/08830189509061743.

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30

Rostaing, Lionel, and Paolo Malvezzi. "Costimulation Blockade in Kidney Transplantation." Transplantation 100, no. 12 (December 2016): 2516–18. http://dx.doi.org/10.1097/tp.0000000000001456.

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31

Malvezzi, Paolo, Thomas Jouve, and Lionel Rostaing. "Costimulation Blockade in Kidney Transplantation." Transplantation 100, no. 11 (November 2016): 2315–23. http://dx.doi.org/10.1097/tp.0000000000001344.

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32

Appleman, Leonard J., and Vassiliki A. Boussiotis. "T cell anergy and costimulation." Immunological Reviews 192, no. 1 (April 2003): 161–80. http://dx.doi.org/10.1034/j.1600-065x.2003.00009.x.

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33

Kirk, Allan D., Douglas K. Tadaki, He Xu, Eric A. Elster, Linda C. Burkley, Abbie Celniker, D. Scott Batty, et al. "PRIMATE ALLOTRANSPLANTATION USING COSTIMULATION BLOCKADE." Transplantation 69, Supplement (April 2000): S414. http://dx.doi.org/10.1097/00007890-200004271-01156.

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34

Arbiser, Jack L., Adam Bingaman, Megan Durham, Shannon Cowan, Cynthia Cohen, Elham Zarnegar, Vijay Varma, and Christian P. Larsen. "SVR Angiosarcomas can be Rejected by CD4 Costimulation Dependent and CD8 Costimulation Independent Pathways." Molecular Medicine 8, no. 9 (September 2002): 551–58. http://dx.doi.org/10.1007/bf03402165.

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35

Wang, Shengdian, Gefeng Zhu, Andrei I. Chapoval, Haidong Dong, Koji Tamada, Jian Ni, and Lieping Chen. "Costimulation of T cells by B7-H2, a B7-like molecule that binds ICOS." Blood 96, no. 8 (October 15, 2000): 2808–13. http://dx.doi.org/10.1182/blood.v96.8.2808.h8002808_2808_2813.

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This report describes a new human B7-like gene designatedB7-H2. Cell surface expression of B7-H2 protein is detected in monocyte-derived immature dendritic cells. Soluble B7-H2 and immunoglobulin (Ig) fusion protein, B7-H2Ig, binds activated but not resting T cells and the binding is abrogated by inducible costimulator Ig (ICOSIg), but not CTLA4Ig. In addition, ICOSIg stains Chinese hamster ovary cells transfected with B7-H2 gene. By suboptimal cross-linking of CD3, costimulation of T-cell proliferation by B7-H2Ig is dose-dependent and correlates with secretion of interleukin (IL)-2, whereas optimal CD3 ligation preferentially stimulates IL-10 production. The results indicate that B7-H2 is a putative ligand for the ICOS T-cell molecule.

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36

Semple, Kenrick, Antony Nguyen, Yu Yu, Honglin Wang, Claudio Anasetti, and Xue-Zhong Yu. "Strong CD28 costimulation suppresses induction of regulatory T cells from naive precursors through Lck signaling." Blood 117, no. 11 (March 17, 2011): 3096–103. http://dx.doi.org/10.1182/blood-2010-08-301275.

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Abstract CD28 costimulation is required for the generation of naturally derived regulatory T cells (nTregs) in the thymus through lymphocyte-specific protein tyrosine kinase (Lck) signaling. However, it is not clear how CD28 costimulation regulates the generation of induced Tregs (iTregs) from naive CD4 T-cell precursors in the periphery. To address this question, we induced iTregs (CD25+Foxp3+) from naive CD4 T cells (CD25−Foxp3−) by T-cell receptor stimulation with additional transforming growth factorβ (TGFβ) in vitro, and found that the generation of iTregs was inversely related to the level of CD28 costimulation independently of IL-2. Using a series of transgenic mice on a CD28-deficient background that bears wild-type or mutated CD28 in its cytosolic tail that is incapable of binding to Lck, phosphoinositide 3-kinase (PI3K), or IL-2–inducible T-cell kinase (Itk), we found that CD28-mediated Lck signaling plays an essential role in the suppression of iTreg generation under strong CD28 costimulation. Furthermore, we demonstrate that T cells with the CD28 receptor incapable of activating Lck were prone to iTreg induction in vivo, which contributed to their reduced ability to cause graft-versus-host disease. These findings reveal a novel mechanistic insight into how CD28 costimulation negatively regulates the generation of iTregs, and provide a rationale for promoting T-cell immunity or tolerance by regulating Tregs through targeting CD28 signaling.

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37

Semple, Kenrick, Antony Nguyen, Yu Yu, Claudio Anasetti, and Xue-Zhong Yu. "Strong CD28 Costimulation Suppresses Induction of Regulatory T Cells From Naïve Precursors through Lck Signaling." Blood 116, no. 21 (November 19, 2010): 3728. http://dx.doi.org/10.1182/blood.v116.21.3728.3728.

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Abstract Abstract 3728 CD28 costimulation is required for the generation of naturally-derived regulatory T cells (nTregs) in the thymus through Lck-signaling. However, it is not clear how CD28 costimulation regulates the generation of induced Tregs (iTregs) from naïve CD4 T-cell precursors in the periphery. To address this question, we induced iTregs (CD25+Foxp3+) from naïve CD4 T cells (CD25−Foxp3−) by TCR-stimulation with additional TGFβ in vitro, and found that the generation of iTregs was inversely related to the level of CD28 costimulation independently of IL-2. By using a series of transgenic mice on CD28-deficient background that bears WT CD28 or mutated CD28 in its cytosolic tail incapable of binding to Lck, PI3K or Itk, we found that CD28-mediated Lck-signaling plays an essential role in the suppression of iTreg generation under strong CD28 costimulation. Furthermore, we demonstrate that T cells with the CD28 receptor incapable of activating Lck were prone to iTreg induction in vivo, which contributed to their reduced ability to cause graft-versus-host disease. These findings reveal a novel mechanistic insight into how CD28 costimulation negatively regulates the generation of iTregs, and provide the rationale for promoting T-cell immunity or tolerance by regulating Tregs through targeting CD28-signaling. Disclosures: No relevant conflicts of interest to declare.

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38

Härtel, Christoph, Lutz Fricke, Nina Schumacher, Holger Kirchner, and Michael Müller-Steinhardt. "Delayed Cytokine mRNA Expression Kinetics after T-Lymphocyte Costimulation: A Quantitative Measure of the Efficacy of Cyclosporin A-based Immunosuppression." Clinical Chemistry 48, no. 12 (December 1, 2002): 2225–31. http://dx.doi.org/10.1093/clinchem/48.12.2225.

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Abstract Background: Because cyclosporin A (CsA) and glucocorticoids inhibit the production of interleukin-2 (IL-2) and other cytokines, quantitative analysis of cytokine mRNA might constitute a pharmacodynamic measure for immunosuppressive drug effects. We investigated whether immunosuppressive drugs influence cytokine mRNA expression kinetics during T-cell costimulation. Methods: We used a human whole blood assay to determine basal (unstimulated) IL-2, IL-4, and tumor necrosis factor-α (TNF-α) mRNA concentrations and expression kinetics after anti-CD3/anti-CD28 monoclonal antibody costimulation in kidney transplant recipients undergoing CsA-based immunosuppressive triple therapy and in healthy controls (ex vivo study I). The effect of CsA on IL-2 mRNA expression kinetics was also determined ex vivo in patients undergoing CsA monotherapy (ex vivo study II) and after in vitro addition of CsA. Results: In ex vivo study I, basal TNF-α mRNA but not IL-2 and IL-4 mRNA was decreased in kidney transplant patients. We observed shifts in peak IL-2 and IL-4 (from 8 to 24 h) and TNF-α (from 4 to 8 h of costimulation) mRNA expression in kidney transplant patients after T-cell costimulation. In patients undergoing CsA monotherapy (ex vivo study II), the inhibitory effect of CsA was detectable as an individually delayed increase in IL-2 mRNA during costimulation. In vitro addition of CsA also induced a dose-independent displacement of IL-2 mRNA expression kinetics (i.e., a delay). Conclusions: A delayed increase in cytokine mRNA expression during T-cell costimulation may represent a sensitive effect of immunosuppression. The single analysis of one absolute or peak mRNA value could be misleading. For prospective studies involving measurement of cytokine mRNA, we therefore suggest the parameter “area of cytokine mRNA expression over time”, which should include absolute cytokine mRNA values at two different time points of mRNA kinetics.

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Wang, Shengdian, Gefeng Zhu, Andrei I. Chapoval, Haidong Dong, Koji Tamada, Jian Ni, and Lieping Chen. "Costimulation of T cells by B7-H2, a B7-like molecule that binds ICOS." Blood 96, no. 8 (October 15, 2000): 2808–13. http://dx.doi.org/10.1182/blood.v96.8.2808.

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Abstract This report describes a new human B7-like gene designatedB7-H2. Cell surface expression of B7-H2 protein is detected in monocyte-derived immature dendritic cells. Soluble B7-H2 and immunoglobulin (Ig) fusion protein, B7-H2Ig, binds activated but not resting T cells and the binding is abrogated by inducible costimulator Ig (ICOSIg), but not CTLA4Ig. In addition, ICOSIg stains Chinese hamster ovary cells transfected with B7-H2 gene. By suboptimal cross-linking of CD3, costimulation of T-cell proliferation by B7-H2Ig is dose-dependent and correlates with secretion of interleukin (IL)-2, whereas optimal CD3 ligation preferentially stimulates IL-10 production. The results indicate that B7-H2 is a putative ligand for the ICOS T-cell molecule.

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Wang, Donghai, Reiko Matsumoto, Yun You, Tuanjie Che, Xue-Yan Lin, Sarah L. Gaffen, and Xin Lin. "CD3/CD28 Costimulation-Induced NF-κB Activation Is Mediated by Recruitment of Protein Kinase C-θ, Bcl10, and IκB Kinase β to the Immunological Synapse through CARMA1." Molecular and Cellular Biology 24, no. 1 (January 1, 2004): 164–71. http://dx.doi.org/10.1128/mcb.24.1.164-171.2003.

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ABSTRACT CARMA1 (also known as CARD11) is a scaffold molecule and contains a caspase-recruitment domain (CARD) and a membrane-associated guanylate kinase-like (MAGUK) domain. It plays an essential role in mediating CD3/CD28 costimulation-induced NF-κB activation. However, the molecular mechanism by which CARMA1 mediates costimulatory signals remains to be determined. Here, we show that CARMA1 is constitutively associated with the cytoplasmic membrane. This membrane association is essential for the function of CARMA1, since a mutant of CARMA1, CARMA1(L808P), that is defective in the membrane association cannot rescue CD3/CD28 costimulation-induced NF-κB activation in JPM50.6 CARMA1-deficient T cells. Although CD3/CD28 costimulation effectively induces the formation of the immunological synapse in CARMA1-deficient T cells, the recruitment of protein kinase C-θ (PKC-θ), Bcl10, and IκB kinase β (IKKβ) into lipid rafts of the immunological synapse is defective. Moreover, expression of wild-type CARMA1, but not CARMA1(L808P), restores the recruitment of PKC-θ, Bcl10, and IKKβ into lipid rafts in CARMA1-deficient T cells. Consistently, expression of a mutant CARMA1, CARMA1(ΔCD), that cannot associate with Bcl10 failed to restore CD3/CD28 costimulation-induced NF-κB activation in JPM50.6 cells, whereas expression of Bcl10-CARMA(ΔCD) fusion protein effectively restored this NF-κB activation. Together, these results indicate that CARMA1 mediates CD3/CD28 costimulation-induced NF-κB activation by recruiting downstream signaling components into the immunological synapse.

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Hatano, Ryo, Kei Ohnuma, Taketo Yamada, Wataru Takasawa, Yuko Endo, Yumiko Matsumura, Osamu Hosono, Nam H. Dang, and Chikao Morimoto. "A Novel Function of CD26-Mediated Costimulation in the Cytotoxic Activity of Human CD8+ T Cells in Xenogeneic Chronic Graft-Versus-Host Disease (cGVHD) and GVL Mice Model." Blood 114, no. 22 (November 20, 2009): 3548. http://dx.doi.org/10.1182/blood.v114.22.3548.3548.

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Abstract Abstract 3548 Poster Board III-485 CD26 is a 110-kDa cell surface glycoprotein with known dipeptidyl peptidase IV (DPPIV) activity in its extracellular domain, capable of cleaving amino-terminal dipeptides with either L-proline or L-alanine at the penultimate position. CD26 activity is dependent on cell type and the microenvironment, which influence its multiple biological roles. CD26 plays an important role in immunology, autoimmunity, diabetes and cancer. The role of CD26 in immune regulation has been extensively characterized, with our recent findings elucidating its linkage with signaling pathways and structures involved in T cells activation as well as antigen presenting cell (APC)-T-cell interaction. CD26 is preferentially expressed on human CD4+ memory T cells and CD4+CD45RO+CD26+ T cells exhibit response maximally to the recall antigen tetanus toxoid. Human T-helper 1 (Th1) cells display a higher expression of CD26 and are much more sensitive to CD26-mediated costimulation than human Th2 cells. In contrast, the role of CD26 in human CD8+ T cells still remains to be elucidated, while CD8+ T cells express CD26 as well as CD4+ T cells. In this study, we studied the effector function of CD26-mediated costimulation of CD8+ T cells. In comparison with CD28-medaited costimulation, which is one of representative T cell costimulatory pathway, CD26-mediated costimulation in CD8+ T cells showed delayed proliferation than that of CD28 stimuatlion, but finally expanded to a similar extent. The secretion of inflammatory cytokines, TNF-alpha and IFN-gamma, was strongly induced after CD26-mediated costimulation. In contrast, the secretion of IL-2 and IL-5 was significantly less as compared with CD28-mediated costimulation. Finally, we showed that the expression of Granzyme B, one of the major effector molecules in the cytotoxic activity of CD8+ T cells, was markedly enhanced by CD26-mediated costimulation in dose dependent manner of anti-CD26 monoclonal antibody stimulation. Moreover, with CD26-mediated costimulation, CD8+ T cells were observed to kill target cells in a Granzyme B-dependent manner. Next, we examined CD26-dependent organ injury by human T cells using xenogeneic chronic GVHD (x-cGVHD) mice model. About 6 weeks after transplantation of human peripheral blood mononuclear cells (PBMC) into NOG-Scid mice, mice develop loss pf hair, loss of weight, and human CD8+ lymphocytes infiltration into liver, lung, and salivary glands, which exhibit pathological changes of cGVHD. Administration of anti-human CD26 mAb decreased onset of x-cGVHD, while human lymphocytes were grafted successfully. Finally, we examined whether GVL effect is exerted via CD26-mediated costimulation, using x-cGVHD mice model in which P388 leukemic cells were grafted subcutaneously. In this tumor-graft model, P388 cells were not grafted in mice with onset of x-cGVHD, which indicated that GVL effect was exerted by human lymphocytes. On the other hand, P388 cells were also diminished in mice with decreased x-cGVHD by administration of anti-CD26 mAb. Taken together, our data strongly suggest that CD26-mediated costimulation in CD8+ T cells deeply involves in the pathology of cGVHD. The present study offers a novel notion that CD26 may become one of therapeutic targets of GVHD without impairment of GVL effect. Disclosures: Yamada: Y's Therapeutics: Membership on an entity's Board of Directors or advisory committees. Dang:Y's Therapeutics: Membership on an entity's Board of Directors or advisory committees, Patents & Royalties. Morimoto:Y's Therapeutics: Patents & Royalties, a board member.

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Riley, James L., and Carl H. June. "The CD28 family: a T-cell rheostat for therapeutic control of T-cell activation." Blood 105, no. 1 (January 1, 2005): 13–21. http://dx.doi.org/10.1182/blood-2004-04-1596.

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Abstract The CD28 family of receptors (CD28, cytotoxic T-lymphocyte–associated antigen 4 [CTLA-4], inducible costimulator [ICOS], program death-1 [PD-1], and B- and T-lymphocyte attenuator [BTLA]) plays a critical role in controlling the adaptive arm of the immune response. While considerable information is available regarding CD28 and CTLA-4, the function of the more recently discovered members of the CD28 family is less well understood. This review will highlight recent findings regarding the CD28 family with special emphasis on effects the CD28 family has on immunopathology, the discovery of costimulatory antibodies with superagonist function, and the status of clinical trials using various strategies to augment or block T-cell costimulation.

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Boussiotis, V. A., D. L. Barber, B. J. Lee, J. G. Gribben, G. J. Freeman, and L. M. Nadler. "Differential association of protein tyrosine kinases with the T cell receptor is linked to the induction of anergy and its prevention by B7 family-mediated costimulation." Journal of Experimental Medicine 184, no. 2 (August 1, 1996): 365–76. http://dx.doi.org/10.1084/jem.184.2.365.

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When stimulated through their antigen receptor, without costimulation, T cells enter a state of antigen-specific unresponsiveness, termed anergy. B7-mediated costimulation, signaling via CD28, is sufficient to prevent the induction of anergy. Here we show that ligation of T cell receptor (TCR) by alloantigen alone, which results in anergy, activates tyrosine phosphorylation of TCR zeta and its association with fyn. In contrast, TCR ligation in the presence of B7 costimulation, which results in productive immunity, activates tyrosine phosphorylation of TCR zeta and CD3 chains, which associate with activated lck and zeta-associated protein (ZAP) 70. Under these conditions, CD28 associates with activated lck and TCR zeta. These data suggest that the induction of anergy is an active signaling process characterized by the association of TCR zeta and fyn. In addition, CD28-mediated costimulation may prevent the induction of anergy by facilitating the effective association of TCR zeta and CD3 epsilon with the critical protein tyrosine kinase lck, and the subsequent recruitment of ZAP-70. Strategies to inhibit or activate TCR-associated, specific protein tyrosine kinase-mediated pathways may provide a basis for drug development with potential applications in the fields of transplantation, autoimmunity, and tumor immunity.

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Lea-Carnall, Caroline A., Nelson J. Trujillo-Barreto, Marcelo A. Montemurro, Wael El-Deredy, and Laura M. Parkes. "Evidence for frequency-dependent cortical plasticity in the human brain." Proceedings of the National Academy of Sciences 114, no. 33 (August 1, 2017): 8871–76. http://dx.doi.org/10.1073/pnas.1620988114.

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Frequency-dependent plasticity (FDP) describes adaptation at the synapse in response to stimulation at different frequencies. Its consequence on the structure and function of cortical networks is unknown. We tested whether cortical “resonance,” favorable stimulation frequencies at which the sensory cortices respond maximally, influenced the impact of FDP on perception, functional topography, and connectivity of the primary somatosensory cortex using psychophysics and functional imaging (fMRI). We costimulated two digits on the hand synchronously at, above, or below the resonance frequency of the somatosensory cortex, and tested subjects’ accuracy and speed on tactile localization before and after costimulation. More errors and slower response times followed costimulation at above- or below-resonance, respectively. Response times were faster after at-resonance costimulation. In the fMRI, the cortical representations of the two digits costimulated above-resonance shifted closer, potentially accounting for the poorer performance. Costimulation at-resonance did not shift the digit regions, but increased the functional coupling between them, potentially accounting for the improved response time. To relate these results to synaptic plasticity, we simulated a network of oscillators incorporating Hebbian learning. Two neighboring patches embedded in a cortical sheet, mimicking the two digit regions, were costimulated at different frequencies. Network activation outside the stimulated patches was greatest at above-resonance frequencies, reproducing the spread of digit representations seen with fMRI. Connection strengths within the patches increased following at-resonance costimulation, reproducing the increased fMRI connectivity. We show that FDP extends to the cortical level and is influenced by cortical resonance.

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Cardoso, Angelo A., Mark J. Seamon, Hernani M. Afonso, Paolo Ghia, Vassiliki A. Boussiotis, Gordon J. Freeman, John G. Gribben, Stephen E. Sallan, and Lee M. Nadler. "Ex Vivo Generation of Human Anti–Pre-B Leukemia-Specific Autologous Cytolytic T Cells." Blood 90, no. 2 (July 15, 1997): 549–61. http://dx.doi.org/10.1182/blood.v90.2.549.549_549_561.

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In contrast to other neoplasms, antigen-specific autologous cytolytic T cells have not been detected in patients with human pre-B–cell leukemias. The absence of efficient B7 family (B7-1/CD80; B7-2/CD86) -mediated costimulation has been shown to be a major defect in tumor cells' capacity to function as antigen-presenting cells. We show here the generation of autologous anti–pre-B–cell leukemia-specific cytolytic T-cell lines from the marrows of 10 of 15 patients with pre-B–cell malignancies. T-cell costimulation via CD28 is an absolute requirement for the generation of these autologous cytolytic T cells (CTL). Although costimulation could be delivered by either bystander B7 transfectants or professional antigen-presenting cells (indirect costimulation), optimal priming and CTL expansion required that the costimulatory signal was expressed by the tumor cell (direct costimulation). These anti–pre-B–cell leukemia-specific CTL lysed both unstimulated and CD40-stimulated tumor cells from each patient studied but did not lyse either K562 or CD40-stimulated allogeneic B cells. Cytolysis was mediated by the induction of tumor cell apoptosis by CD8+ T cells via the perforin-granzyme pathway. Although we were able to generate anti–leukemia-specific CTL from the bone marrow, we were unable to generate such CTL from the peripheral blood of these patients. These studies show that antigen-specific CTL can be generated from the bone marrow of patients with pre-B–cell leukemias and these findings should facilitate the design of adoptive T-cell–mediated immunotherapy trials for the treatment of patients with B-cell precursor malignancies.

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Yu, Guang, Hongyu Luo, Yulian Wu, and Jiangping Wu. "Ephrin B2 Induces T Cell Costimulation." Journal of Immunology 171, no. 1 (July 1, 2003): 106–14. http://dx.doi.org/10.4049/jimmunol.171.1.106.

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Jenkins, Marc K., and Julia G. Johnson. "Molecules involved in T-cell costimulation." Current Opinion in Immunology 5, no. 3 (June 1993): 361–67. http://dx.doi.org/10.1016/0952-7915(93)90054-v.

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Ward, S. "Immunological synapse generates microenvironment for costimulation." Trends in Immunology 23, no. 4 (April 1, 2002): 177–78. http://dx.doi.org/10.1016/s1471-4906(02)02176-2.

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Liew, F. Y. "A toll for T cell costimulation." Annals of the Rheumatic Diseases 63, suppl_2 (November 1, 2004): ii76—ii78. http://dx.doi.org/10.1136/ard.2004.028308.

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Maltzman, J. S. "Costimulation Blockade-A Double-Edged Sword?" American Journal of Transplantation 12, no. 9 (August 27, 2012): 2269–70. http://dx.doi.org/10.1111/j.1600-6143.2012.04185.x.

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