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Relevant bibliographies by topics / Recepteur cellule t

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Academic literature on the topic 'Recepteur cellule t'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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Journal articles on the topic "Recepteur cellule t"

1

Camani, Chantal, Olivier Gavin, and Egbert Kruithof. "Cellular Degradation of Free and Inhibitor-bound Tissue-type Plasminogen Activator." Thrombosis and Haemostasis 83, no. 02 (2000): 290–96. http://dx.doi.org/10.1055/s-0037-1613801.

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SummaryThe low density lipoprotein receptor-related protein (LRP) is a multiligand clearance receptor that removes free tissue-type plasminogen activator (t-PA) or complexes of t-PA with plasminogen activator inhibitor type 1 (PAI-1) from the blood circulation or the pericellular space. Co-receptors are essential for LRP-mediated clearance of several ligands (e.g. glycosaminoglycans for thrombin/protease nexin and lipoprotein lipase, and the urokinase receptor for urokinase/PAI-1 complexes). The present study was undertaken to investigate whether LRP-mediated t-PA clearance requires a co-receptor as well.In five cell lines from different organs and species degradation of t-PA and t-PA/PAI-1 was mediated by LRP (or LRP-like receptors). No degradation of t-PA and t-PA/PAI-1 occurred in THP-1 or U-937 human monocyte-like cells, despite the presence of functional LRP. As glycosaminoglycans can bind t-PA and PAI-1 we investigated whether they are involved in t-PA/PAI-1 degradation. Pre-treatment of COS cells or HT1080 cells with chlorate, an inhibitor of glycosaminoglycan sulfation, did not decrease t-PA/PAI-1 degradation. Furthermore, CHO cells genetically deficient in glycosaminoglycans efficiently degraded t-PA/PAI-1. Thus it is unlikely that glycosaminoglycans are co-receptors for degradation of t-PA or t-PA/PAI-1.This study indicates that THP-1 and U-937 cells lack a critical component (co-receptor?) for the LRP-mediated degradation of t-PA. Abbreviations: LRP, low density lipoprotein receptor-related protein; PAI-1, plasminogen activator inhibitor type 1; RAP, receptor-associated protein; t-PA, tissue-type plasminogen activator; u-PA, urokinase; u-PAR, urokinase receptor.

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Marin, Ana V. M., Beatriz Garcillán, Anaïs Jiménez-Reinoso, Miguel Muñoz-Ruiz, Alejandro C. Briones, Edgar Fernández-Malavé, Maria J. Recio, and José R. Regueiro. "Human congenital T-cell receptor disorders." LymphoSign Journal 2, no. 1 (March 1, 2015): 3–19. http://dx.doi.org/10.14785/lpsn-2014-0012.

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Immunodeficiencies of most T-cell receptor (TCR) components (TCRID) have been reported in almost 40 patients worldwide who have also, at times, shown signs of autoimmunity. We updated their clinical, immunological, and molecular features with an emphasis on practical diagnosis, as the range of the disorder grows in complexity with new partial defects. Cellular and animal models are also reviewed and in some cases reveal their limitations for predicting TCRID immunopathology.

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Morctta, Lorenzo, Ermanno Ciccone, Silvano Ferrini, Pier Giuseppe Pelicci, Maria Cristina Mingari, Jan Zeromski, Cristina Bottino, Carlo Grossi, and Alessandro Moretta. "Molecular and Cellular Analysis of Human T Lymphocytes Expressing gammadelta T-Cell Receptor." Immunological Reviews 120, no. 1 (April 1991): 117–35. http://dx.doi.org/10.1111/j.1600-065x.1991.tb00590.x.

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Hamrouni, Abdelbasset, Anna Olsson, G. Jan Wiegers, and Andreas Villunger. "Impact of cellular lifespan on the T cell receptor repertoire." European Journal of Immunology 37, no. 7 (June 11, 2007): 1978–85. http://dx.doi.org/10.1002/eji.200636632.

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Lai, Kar Neng, Joseph C. K. Leung, Chun Chung Chow, and Clive S. Cockram. "T lymphocyte activation in euthyroid Graves' ophthalmopathy: soluble interleukin 2 receptor release, cellular interleukin 2 receptor expression and interleukin 2 production." Acta Endocrinologica 120, no. 5 (May 1989): 602–9. http://dx.doi.org/10.1530/acta.0.1200602.

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Abstract. The present study was undertaken to examine the cellular control arm of the immune response with regard to T lymphocyte proliferation in euthyroid Graves' ophthalmopathy. Twenty patients with euthyroid Graves' ophthalmopathy (7 on antithyroid drugs and 13 on no treatment) and 18 healthy controls were studied in an infection-free period. Mitogen-stimulated cellular interleukin 2 (IL2) receptor expression, soluble interleukin 2 receptor release, and interleukin 2 production, were studied in peripheral blood mononuclear cells cultured for 24 h. The cellular IL2 receptor expression and soluble IL2 receptor release did not differ between the patients and healthy controls. In contrast, IL2 production in response to pokeweed mitogen stimulation was increased in lymphocytes from patients with Graves' ophthalmopathy. The IL2 release did not correlate with the quantities of cellular and soluble IL2 receptor. The mitogen-stimulated cellular IL2 receptor expression, IL2 receptor release, and IL2 production did not differ between patients with or without carbimazole therapy. Despite a suggested role of autoreactive T cells in mediating the development and propagation of autoimmune thyroid disease, this study fails to demonstrate a defective T lymphocyte activation state in patients with Graves' ophthalmopathy during an euthyroid state.

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Clémenceau, Béatrice, Nicolas Congy-Jolivet, Géraldine Gallot, Régine Vivien, Joëlle Gaschet, Gilles Thibault, and Henri Vié. "Antibody-dependent cellular cytotoxicity (ADCC) is mediated by genetically modified antigen-specific human T lymphocytes." Blood 107, no. 12 (June 15, 2006): 4669–77. http://dx.doi.org/10.1182/blood-2005-09-3775.

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AbstractIn the context of transplantation, donor and virus-specific T-lymphocyte infusions have demonstrated the dramatic potential of T cells as immune effectors. Unfortunately, most attempts to exploit the T-cell immune system against nonviral malignancies in the syngeneic setting have been disappointing. In contrast, treatments based on monoclonal antibodies (Abs) have been clinically successful and have demonstrated the clinical relevance of several antigens as therapeutic targets and the importance of the antibody-dependent cellular cytotoxicity (ADCC) pathway. In the present study, we considered the possibility of arming specific T cells with a receptor that would enable them to mediate ADCC. After transduction with a CD16/γ receptor gene, CD4+ and CD8+ cytotoxic T lymphocytes displayed stable expression of the CD16 receptor at their surface. In the absence of Ab, CD16/γ expression did not affect the capacity of specific T lymphocytes to kill their target following “natural” T-cell receptor recognition. When tested against the autologous B-lymphoblastoid cell line (BLCL) coated with anti-CD20 mAb, the newly expressed Fc receptor enabled the T cells to kill the BLCL through ADCC. Adoptive transfer of such newly designed immune effector may be considered to increase antibody efficiency by harnessing the immune potential of T cells.

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Guedan, Sonia, Marco Ruella, and Carl H. June. "Emerging Cellular Therapies for Cancer." Annual Review of Immunology 37, no. 1 (April 26, 2019): 145–71. http://dx.doi.org/10.1146/annurev-immunol-042718-041407.

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Genetically engineered T cells are powerful new medicines, offering hope for curative responses in patients with cancer. Chimeric antigen receptor (CAR) T cells were recently approved by the US Food and Drug Administration and are poised to enter the practice of medicine for leukemia and lymphoma, demonstrating that engineered immune cells can serve as a powerful new class of cancer therapeutics. The emergence of synthetic biology approaches for cellular engineering provides a broadly expanded set of tools for programming immune cells for enhanced function. Advances in T cell engineering, genetic editing, the selection of optimal lymphocytes, and cell manufacturing have the potential to broaden T cell–based therapies and foster new applications beyond oncology, in infectious diseases, organ transplantation, and autoimmunity.

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Griffioen, Marieke, H. M. Esther van Egmond, Menno A. W. G. van der Hoorn, Renate S. Hagedoorn, Michel Kester, Roelof Willemze, J. H. Frederik Falkenburg, and Mirjam Heemskerk. "T Cell Receptor Gene Transfer to Virus-Specific T Cells for Cellular Anti-Tumor Immunotherapy." Blood 110, no. 11 (November 16, 2007): 2594. http://dx.doi.org/10.1182/blood.v110.11.2594.2594.

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Abstract Patients with relapsed hematological malignancies after allogeneic stem cell transplantation (alloSCT) can be successfully treated by donor lymphocyte infusions (DLI). Since DLI consists of a variety of T cells with different specificities, the benificial anti-leukemic effect of DLI is often accompanied by Graft-versus-Host Disease (GvHD). Genetic modification of T cells to express T cell receptors (TCR) with defined anti-tumor specificity would be an attractive strategy to specifically eradicate the malignant cells without induction of GvHD. We previously demonstrated that transfer of the minor histocompatibility antigen HA-2 specific TCR to CMV specific T cells led to the generation of T cells with dual specificity for CMV as well as HA-2. CMV and EBV specific T cells are ideal target cells for TCR gene transfer, since the majority of human individuals have high frequencies of these T cells due to latent persistence of CMV and EBV. In addition, based on their virus specificity, these T cells do not induce GvHD in an alloSCT setting, and we hypothesize that due to frequent encounter with viral antigens, TCR transferred virus specific T cells will survive for a prolonged period of time in vivo. The aim of this study is to develop a clinical grade method for the generation of TCR transduced virus specific T cells for cellular immunotherapy. CMV and EBV specific T cells were isolated from healthy individuals using pentamers in combination with clinical grade available anti-biotin magnetic beads. Isolation by pentamer-coated beads induced stimulation, expansion and efficient transduction of virus specific T cells, leading to the generation of cell lines with high frequencies of virus specific (>80%) and transduced (20–40%) T cells. T cells were transduced with multi-cistronic retroviral vectors encoding the α and β chains of the HA-2 TCR linked by an IRES or 2A-like sequence. No differences in transduction efficiency and TCR surface expression were observed between the IRES and 2A-like vectors. The transduced virus specific T cells were shown to exhibit dual specificity and tetramer staining of the introduced TCR correlated with specific lysis of target cells endogenously-expressing HA-2. Furthermore, variation in surface expression of the introduced TCR was observed between T cells with different virus specificities. T cells directed against the HLA-A1 epitope of CMV-pp50, for example, efficiently expressed the HA-2 TCR, whereas T cells specific for the HLA-B8 epitope of EBV-EBNA-3A did not express the introduced TCR. Functional analyses demonstrated that TCR-transduced pp50 specific T cells were dual specific, recognizing HA-2 as well as pp50 positive target cells, whereas TCR-engineered EBNA-3A specific T cells were primarily EBNA-3A specific. The efficiency of surface expression of the transferred TCR was shown to be determined by intrinsic properties of the TCRs, illustrating that for TCR gene transfer purposes TCRs need to be selected that exhibit high competition potential, whereas recipient T cells need to express endogenous TCRs with low competition potential. For clinical application, TCRs will be transferred to virus specific T cells selected for their capacity to efficiently express the introduced TCR without loss of virus specificity. The safety, clinical and immunological efficacy of TCR gene transfer to virus specific T cells as cellular anti-tumor immunotherapy after alloSCT will be investigated in a clinical phase I/II study.

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Ittershagen, Stacie, Solveig Ericson, Lamis Eldjerou, Ali Shojaee, Eric Bleickardt, Manisha Patel, Tetiana Taran, et al. "Industry’s Giant Leap Into Cellular Therapy: Catalyzing Chimeric Antigen Receptor T Cell (CAR-T) Immunotherapy." Current Hematologic Malignancy Reports 14, no. 1 (January 21, 2019): 47–55. http://dx.doi.org/10.1007/s11899-019-0498-6.

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Currie, James, Mario Castro, Grant Lythe, Ed Palmer, and Carmen Molina-París. "A stochastic T cell response criterion." Journal of The Royal Society Interface 9, no. 76 (June 28, 2012): 2856–70. http://dx.doi.org/10.1098/rsif.2012.0205.

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The adaptive immune system relies on different cell types to provide fast and coordinated responses, characterized by recognition of pathogenic challenge, extensive cellular proliferation and differentiation, as well as death. T cells are a subset of the adaptive immune cellular pool that recognize immunogenic peptides expressed on the surface of antigen-presenting cells by means of specialized receptors on their membrane. T cell receptor binding to ligand determines T cell responses at different times and locations during the life of a T cell. Current experimental evidence provides support to the following: (i) sufficiently long receptor–ligand engagements are required to initiate the T cell signalling cascade that results in productive signal transduction and (ii) counting devices are at work in T cells to allow signal accumulation, decoding and translation into biological responses. In the light of these results, we explore, with mathematical models, the timescales associated with T cell responses. We consider two different criteria: a stochastic one (the mean time it takes to have had N receptor–ligand complexes bound for at least a dwell time, τ , each) and one based on equilibrium (the time to reach a threshold number N of receptor–ligand complexes). We have applied mathematical models to previous experiments in the context of thymic negative selection and to recent two-dimensional experiments. Our results indicate that the stochastic criterion provides support to the thymic affinity threshold hypothesis, whereas the equilibrium one does not, and agrees with the ligand hierarchy experimentally established for thymic negative selection.

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Dissertations / Theses on the topic "Recepteur cellule t"

1

Halary, Franck. "Etude des lymphocytes t gamma/delta humains : aspect du controle des fonctions biologiques et de la specificite antigenique (doctorat : immunologie)." Nantes, 1999. http://www.theses.fr/1999NANT10VS.

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2

TILLOY, FLORENCE. "Etude des sous-populations lymphocytaires t exprimant les chaines alpha invariantes du tcr : ontogenie des cellules t-nk et mise en evidence d'une nouvelle sous-population conservee chez les mammiferes." Paris 5, 1999. http://www.theses.fr/1999PA05N097.

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Mancini, Stéphane. "Différenciation des lymphocytes T et recombinaison des gènes du TCR : quel rôle pour le pré-TCR dans la régulation du réarrangement des gènes codant pour la chaîne [alpha] du TCR ?" Université Joseph Fourier (Grenoble), 2000. http://www.theses.fr/2000GRE10116.

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Les genes codant pour les chaines alpha et beta du recepteur a l'antigene des cellules t (tcr) sont rearranges sequentiellement durant la differenciation intrathymique des lymphocytes t, caracterisee par l'expression de plusieurs molecules membranaires, dont cd4 et cd8. Le rearrangement des genes tcrb, codant pour la chaine beta, intervient durant le stade cd4 8 (dn), et permet l'expression d'un pre-tcr comprenant la chaine beta, ptalpha et le complexe cd3, responsable de la transduction des signaux d'activation. L'assemblage du pre-tcr induit la maturation des thymocytes jusqu'au stade cd4 +8 + (dp). Il est generalement admis que les genes tcra, codant pour la chaine alpha, sont rearranges a la transition dn/dp, apres signalisation par le pre-tcr. Ma these a pour objet l'etude de la regulation des rearrangements des genes tcra, et du role du pre-tcr dans ce processus. L'inactivation du gene codant pour ptalpha entraine chez la souris un blocage partiel de la differenciation des lymphocytes t au stade dn. Nous avons montre que le repertoire des chaines tcralpha exprimees chez ces animaux est essentiellement normal. Il semble donc que le pre-tcr ne soit pas requis pour le rearrangement et l'expression des genes tcra, et que ces evenements peuvent potentiellement se produire au stade dn. Nous avons poursuivi ces travaux en analysant le statut des genes tcra dans d'autres modeles de souris genetiquement modifiees ou la differenciation des thymocytes est bloquee au stade dn. Nous avons pu formellement demontrer, pour la premiere fois, la presence de rearrangements tcra des le stade dn, en absence de signaux issus de cd3, du pre-tcr ou du tcr. Enfin, nous avons etudie la reponse a l'irradiation des thymocytes de souris n'exprimant pas cd3. L'irradiation conduit a l'induction des rearrangements tcra et a la reprise de la differenciation a la fois par des voies p53 dependantes et independantes.

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Vigan, Finlin Ines Nadège. "Caractéristiques phénotypiques et fonctionnelles des lymphocytes T intra-hépatiques et périphériques au cours de l'hépatite virale chronique C." Université Joseph Fourier (Grenoble), 2001. http://www.theses.fr/2001GRE10117.

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L'hepatite virale c (hvc) represente un reel probleme de sante publique compte tenu de sa prevalence et du risque important d'evolution vers la cirrhose et le carcinome hepato-cellulaire. Ma these a pour objet de caracteriser la diversite, le phenotype et la fonction des populations lymphocytaires t intra-hepatiques et peripheriques au cours de l'hepatite chronique virale c. Nous avons evalue la diversite des lymphocytes t + intra-hepatiques et peripheriques, par analyse moleculaire de l'heterogeneite des regions hypervariables cdr3 des transcrits codant pour la chaine du recepteur a l'antigene des lymphocytes t(tcr). Cette etude montre que les lymphocytes t intra-hepatiques expriment une grande diversite de tcr. La reponse immune intra-hepatique developpee par l'hote au cours de la pathologie est de type polyclonale et multi-specifique. Nous avons ensuite etudie par cytometrie de flux et rt-pcr quantitative les caracteristiques phenotypiques et fonctionnelles des populations lymphocytaires t intra-hepatiques et peripheriques et ce en relation avec les parametres virologiques, histologiques et biochimiques des patients infectes par le virus de l'hepatite c. L'analyse par cytometrie montre une correlation etroite et significative entre la frequence de lymphocytes conventionnels cd3 +cd56 - intra hepatiques et les marqueurs de la severite de la maladie (scores histologiques de knodell et de metavir, et le taux de transaminases). Une correlation significative a egalement ete retrouvee entre le lymphocytes t cd3 +cd56 - peripheriques et les marqueurs de la severite de la maladie. L'analyse par rt-pcr quantitative des transcrits specifiques des populations lymphocytaires t montre que les quantites de transcrits cd3, tcr, cd8, cd69, perforine et plus particulierement celle des transcrits cd8 sont significativement correlees au taux de transaminases, au score de knodell et a l'index d'activite metavir. Ces resultats renforcent ceux obtenus par cytomertrie et suggerent une fois de plus un role deletere des lymphocytes t conventionnels cd3 +tcr +cd8 + intra-hepatiques au cours de la phase chronique de la pathologie.

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CHEVALIER, SYLVIE. "Etude de la tolerance induite par des transfusions sanguines dans un modele de rat : etude de la forme soluble du recepteur a l'il2 dans un modele de rat, etude du deuxieme recepteur t : tcr gamma/delta chez l'homme." Nantes, 1988. http://www.theses.fr/1988NANT2011.

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Hoghoughi, Neda. "Caractérisation fonctionnelle d'une nouvelle translocation t(3;5)(q21;q31), ciblant le gène du récepteur aux glucocorticoïde et un ARN non-codant, dans la leucémie aigüe à cellules plasmocytoides dendritiques." Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENV073/document.

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La leucémie aiguë à cellules dendritiques plasmacytoïdes (BPDCN) fait partie des cancers incurables pour lesquels les mécanismes impliqués dans la pathogénèse restent inconnus. Dans ce travail, nous avons identifié le gène NR3C1 (5q31), qui code pour le récepteur des glucocorticoïdes (GCR), et un long ARN non-codant inter-génique (appelé ici lincRNA-3q), comme étant des cibles d'altération géniques ou de dérégulation transcriptionnelles dans les BPDCN. La translocation/délétion de NR3C1 est associée avec un temps de survie extrêmement court et des activités anormales du réseau de régulation des gènes GCR, EZH2 et FOXP3. Nous avons découvert que lincRNA-3q code pour une forme nucléaire d'ARN non-codant qui est activé de façon ectopique dans les BPDCN et les AML à haut risque. Dans les cancers myéloïdes, une déplétion de lincRNA-3q induit un arrêt du cycle cellulaire qui coïncide avec la suppression des signatures d'expression génique de E2F1/Rb et des gènes spécifiques aux cellules souches leucémiques. Nos résultats démontrent qu'une inhibition des protéines à bromodomaine BET supprime sélectivement l'expression lincRNA-3q, indiquant une stratégie thérapeutique potentielle pour contrer l'activité oncogénique de cet ARN non-codant. Ce travail défini, un nouveau cadre de recherche pour comprendre la pathogénèse et la résistance au traitement dans les BPDCN
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an incurable malignancy for which disease mechanisms are unknown. Here, we identify the NR3C1 gene (5q31), encoding the glucocorticoid receptor (GCR), and a long, intergenic, non-coding RNA gene (named here lincRNA-3q), respectively, as targets for genetic alteration or transcriptional deregulation in BPDCN. NR3C1 translocation/deletion was associated to critically short survival in BPDCN and to abnormal activity of GCR, EZH2, and FOXP3 gene regulatory networks. LincRNA-3q, was found to encode a nuclear, non- coding RNA that is ectopically activated in BPDCN and high-risk AML. Depletion of lincRNA-3q in myeloid cancer cells induced cell cycle arrest, coincident to suppression of E2F1/Rb and leukemia stem cell-specific gene expression signatures. BET bromodomain protein inhibition could selectively suppress lincRNA-3q indicating a treatment strategy for counteracting oncogenic activity of this non- coding RNA. Thus, this work defines a new framework for understanding disease pathogenesis and treatment resistance in BPDCN

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Moisan, Jean-Paul. "Etude et caracterisation de marqueurs genetiques specifiques du chromosome x humain (suivi de) etude des rearrangements du recepteur a l'antigene, sur des lymphocites t actives in vivo." Université Louis Pasteur (Strasbourg) (1971-2008), 1987. http://www.theses.fr/1987STR13231.

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Le, Paslier Denis. "Genetique moleculaire de deux familles multigeniques primordiales pour l'immunite : les genes des recepteurs des cellules t pour l'antigene et le complexe majeur d'histocompatibilite chez l'homme." Paris 7, 1988. http://www.theses.fr/1988PA077104.

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Mathieu-Mahul, Danièle. "Analyse moleculaire d'anomalies chromosomiques specifiques d'hemopathies malignes humaines." Paris 7, 1987. http://www.theses.fr/1987PA077133.

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AIFANTIS, IOANNIS. "Analyse du role du recepteur pre-tcr dans le developpement des cellules t." Paris 5, 1999. http://www.theses.fr/1999PA05N085.

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Books on the topic "Recepteur cellule t"

1

Oksenberg, Jorge R. Polymerase chain reaction and the analysis of the t cell receptor repertoire. Austin, Tex: R.G. Landes, 1992.

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John, Stewart. The primordial VRM system and the evolution of vertebrate immunity. Austin: R.G. Landes, 1994.

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(Editor), Dirk Nagorsen, and F. M. Marincola (Editor), eds. Analyzing T Cell Responses: How to analyze cellular immune responses against tumor associated antigens. Springer, 2005.

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B, Sigalov Alexander, ed. Multichain immune recognition receptor signaling: From spatiotemporal organization to human disease. New York: Springer Science+Business Media, 2008.

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H, Kiyono, Jirillo E, De Simone Claudio, and International Conference on Molecular Aspects of Immune Response and Infectious Diseases (1989 : Rome, Italy), eds. Molecular aspects of immune response and infectious diseases. New York: Raven, 1990.

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Book chapters on the topic "Recepteur cellule t"

1

Ferrarini, Marco, Carmen Molina-París, and Grant Lythe. "Sampling from T Cell Receptor Repertoires." In Modeling Cellular Systems, 67–79. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45833-5_3.

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Kabelitz, Dieter, and Daniela Wesch. "T-Cell Receptor Repertoire Analysis by Flow Cytometry." In Cellular Diagnostics, 200–210. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000209163.

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Neagu, Monica, and Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases." In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.

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AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.

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Abraham, Robert T., James A. Augustine, Janis W. Schlager, Thomas J. Barna, and Paul J. Leibson. "Initiation and Modulation of Signal Output from the T cell Antigen Receptor." In Biology of Cellular Transducing Signals, 173–83. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0559-0_18.

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Rotteveel, Francien T. M., and Cornelis J. Lucas. "T Cells in the CSF of MS Patients: Analysis of Oligoclonality with the use of a T-Cell Receptor cDNA Probe." In Cellular and Humoral Immunological Components of Cerebrospinal Fluid in Multiple Sclerosis, 337–43. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-5348-3_38.

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Davis, M. M., D. S. Lyons, J. D. Altman, M. McHeyzer-Williams, J. Hampl, J. J. Boniface, and Y. Chien. "T Cell Receptor Biochemistry, Repertoire Selection and General Features of TCR and Ig Structure." In Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms, 94–104. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515280.ch7.

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Davis, M. M., C. Goodnow, N. R. J. Gascoigne, T. Lindsten, and Y. Chien. "Murine T-Cell Receptor Genes and the Problems of Cellular Recognition and Repertoire Selection." In Regulation of Immune Gene Expression, 137–42. Totowa, NJ: Humana Press, 1986. http://dx.doi.org/10.1007/978-1-4612-5014-2_12.

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Defreitas, Elaine C., M. Sandberg-Wolheim, and Hilary Koprowski. "IL-2 Receptor Expression on T Cell Lines Derived from Peripheral Blood and Cerebrospinal Fluid of Multiple Sclerosis Patients." In Cellular and Humoral Immunological Components of Cerebrospinal Fluid in Multiple Sclerosis, 313–21. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-5348-3_36.

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Spickett, Gavin P. "Cellular investigations." In Oxford Handbook of Clinical Immunology and Allergy, 555–78. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199603244.003.0020.

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Introduction Flow cytometry Tissue culture Proliferation assays Immunohistology Cytokine, chemokine, soluble protein assays Apoptosis assays Adhesion markers Bronchoalveolar lavage (BAL) studies CD40 ligand expression Complement membrane regulatory factors Cytokine and cytokine receptor measurement Cytotoxic T cells FOXP3 (regulatory T cells—IPEX syndrome) Genetic and protein studies...

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Horgan, Carol, and John D. Fraser. "The T cell receptor." In Receptors of Cell Adhesion and Cellular Recognition, 77–104. Elsevier, 1996. http://dx.doi.org/10.1016/s1874-5342(96)80018-3.

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Conference papers on the topic "Recepteur cellule t"

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Chaudhury, Anwesha, Andrew Stein, Stephan Grupp, John Levine, Michael Pulsipher, G. Doug Myers, Edward Waldron, et al. "Abstract 509: Conversion of cellular kinetic data for chimeric antigen receptor T-cell therapy (CAR-T) into interpretable units." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-509.

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Bakhit, C., D. Lewis, R. Billings, and B. Malfroy. "CELLULAR CATABOLISM OF RECOMBINANT TISSUE-TYPE PLASMINOGEN ACTIVATOR: IDENTIFICATION AND CHARACTERIZATION OF A NOVEL HIGH AFFINITY UPTAKE SYSTEM ON RAT HEPATOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644400.

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The uptake, internalization and intracellular degradation of 125I-labeled rt-PA (125I-rt-PA) by isolated rat hepatocytes was investigated. Incubation at 37°C resulted in internalization of 125I-rt-PA, followed by the appearance of labeled trichloroacetic acid-soluble (TCA) material in the inclubation media due to degradation of rt-PA. Degradation of rt-PA was inhibited by the presence of NH4Cl (10mM) or chloroquine (ImM) (lysosoma tropic agents) in the incubation media. This suggests that rt-PA degradation occurs intracellularly, perhaps within the lysosomes. 125I-rt-PA was taken up by rat hepatocytes through a specific, high affinity mechanism. Scatchard analysis of the data indicated that 106 molecules of rt-PA were taken up per cell/hour and the calculated dissociation constant was lOnM. Uptake of 125I-rt-PA was not inhibited by glycopeptides isolated from rt-PA nor by several other glycoproteins known to be cleared by identified hepatic receptors. These results suggest that the uptake of rt-PA by rat hepatocytes involves a receptor specific for t-PA and is not mediated by a carbohydrate specific receptor.

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Belin, D., D. Baccino, A. Wohlwend, A. Estreicher, J. Hurate, and J.-D. Vassalli. "A CELLULAR RECEPTOR FOR UROKINASE-TYPE PLASMINOGEN ACTIVATOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642957.

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Recent cell biological and biochemical studies on the urokinase-type plasminogen activator (u-PA) have revealed an unsuspected property of this protein: it binds with high affinity and specificity to the plasma membrane of a number of cell types. Hence, while the interaction of tissue-type plasminogen activator (t-PA) with fibrin suggests a preferred role for this enzyme in the maintenance of fluidity of the extracellular milieu, the cellular binding of u-PA results in the focalisation of plasmin generation to the close environment of the cell surface; this appears as an optimal configuration if u-PA is to participate in the enzymatic events required for cell migration.The available information on the cellular binding of u-PA can be summarized as follows:1. Human monocytes-macrophages, monocyte-like cell lines, fibroblasts, and a variety of other cell lines all express u-PA binding sites. The number of u-PA binding sites on a given cell type may vary as a function of the functional state of the cells. In some cases all sites are occupied by “endogenous” u-PA.2. Binding does not require u-PA activity, and prou-PA binds with the same affinity as does the active enzyme.3. The Kd for u-PA binding is between 1 and 10×10-10 M. The binding site appears to be specific for u-PA.4. Binding requires the presence of the A chain of u-PA; the growth factor module of the A chain is involved in this interaction.5. Bound enzyme does not dissociate readily, nor is it rapidly endocytosed; most importantly, it retains catalytic activity.Studies in progress are aimed at further defining the u-PA determinants responsible for binding. In this context it is noteworthy that there is a tight species specificity of binding: human and murine u-PA, for instance, bind only to cells of the homologous species. Characterization of the u-PA binding site suggests that it is an integral membrane protein that includes at least one Mf 50.000 polypeptide chain.In addition to allowing for the peri-cellular focalisation of u-PA catalysed proteolysis, expression of the u-PA binding site provides a mecanism whereby one cell type can acquire membrane-bound u-PA activity following secretion of the (pro)enzyme by another cell population. A striking example of this is the binding of u-PA, synthesized by the epithelial layer of the male genital tract, to the head region of murine spermatozoa.

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Bailis, Julie M., Jessica N. Orf, Alexander Sternjak, Brian Belmontes, Ryan Case, Natalia Grinberg, Wesley Chang, Beth Hinkle, and Matthias Friedrich. "Abstract 4999: Cellular mechanism of action of bispecific T-cell engager (BiTE®) antibody constructs targeting Folate Receptor 1." 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.am2016-4999.

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Morrissey, J. H., S. A. Gregory, and T. S. Edgington. "DIFFERENTIAL EXPRESSION AND SUBCELLULAR LOCALIZATION OF TISSUE FACTORIN A CONSTITUTIVE VERSUS AN INDUCIBLE CELL TYPE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643739.

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Tissue factor (TF) is an integral membraneglycoprotein and receptor present on a variety of cells outside of the vasculature, but normally absent from intravascular cells. TF plays a central role in initiation of coagulation by rapidly binding and allosterically activating bound factor Vll/VIIa, which proteoly-tically activates coagulation factors IX and X. This protease cascade appears to play a role in the cellular inflammatory response, during which endothelial cells and monocytes/macrophages can be induced to express cell surface TF.Monocyte TF can be induced in response to endotoxin and also via direct interaction with activated T cells and by a specific lymphokine.We have developed a panel of polyclonaland twenty-nine high affinity monoclonal antibodies to human TF. The antibodies recognize TF epitopes under a broad range of conditions, some of which rapidly and efficiently neutralize <95% of TF activity isolated from brain, placenta and expressed bycultured cells. Using these antibodies in immunohistochemical assays, we haveobserved little or no TF antigen cytologically associated with resting monocytes, noTF activity, and following stimulation, the cytologic appearance of TF antigen parallels the acquisition of TF activity.Immunohistochemical staining of stimulated monocytesis diffuse, consistent with homogeneous cell-surface distribution of the TF molecule.In addition, the normal human fibroblastic cell lines GM1380 and GM1381, whichexpress TF const itutively, show a cytologically different and much more intense pattern of intracellular inclusions of TF. This is consistent with previous observationsthat lysed cells show about five-fold moreTF activity than do intact cells. These findings indicate the presence of an intracellular storage site for TF in some cell types, a pattern presently associated only with constitutive expression of this receptor protein. In addition, they confirm thatTF is induced in stimulated monocytes rather than translocation or modification. Supported by NIH grants HL-16411 and CA-41085.

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