Littérature scientifique sur le sujet « CD30L T cell »
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Articles de revues sur le sujet "CD30L T cell"
Younes, A., U. Consoli, V. Snell, K. Clodi, K. O. Kliche, J. L. Palmer, H. J. Gruss et al. « CD30 ligand in lymphoma patients with CD30+ tumors. » Journal of Clinical Oncology 15, no 11 (novembre 1997) : 3355–62. http://dx.doi.org/10.1200/jco.1997.15.11.3355.
Texte intégralWillis, Cynthia R., Yi-Ling Hu, Anh Leith et James B. Rottman. « CD30 / CD30L interactions promote class-switched antibody responses to T-dependent antigens (34.3) ». Journal of Immunology 182, no 1_Supplement (1 avril 2009) : 34.3. http://dx.doi.org/10.4049/jimmunol.182.supp.34.3.
Texte intégralMori, M., C. Manuelli, N. Pimpinelli, C. Mavilia, E. Maggi, M. Santucci, B. Bianchi, P. Cappugi, B. Giannotti et M. E. Kadin. « CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas : A Clue to the Pathophysiology of Clinical Regression ». Blood 94, no 9 (1 novembre 1999) : 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.
Texte intégralMori, M., C. Manuelli, N. Pimpinelli, C. Mavilia, E. Maggi, M. Santucci, B. Bianchi, P. Cappugi, B. Giannotti et M. E. Kadin. « CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas : A Clue to the Pathophysiology of Clinical Regression ». Blood 94, no 9 (1 novembre 1999) : 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.421k28_3077_3083.
Texte intégralGattei, Valter, Massimo Degan, Annunziata Gloghini, Angela De Iuliis, Salvatore Improta, Francesca Maria Rossi, Donatella Aldinucci et al. « CD30 Ligand Is Frequently Expressed in Human Hematopoietic Malignancies of Myeloid and Lymphoid Origin ». Blood 89, no 6 (15 mars 1997) : 2048–59. http://dx.doi.org/10.1182/blood.v89.6.2048.
Texte intégralRottman, James B., Yi-Ling Hu et Cynthia Willis. « Blockade of the CD30/CD30L pathway inhibits renal disease in young, SLE-prone NZB/W F1 mice (50.41) ». Journal of Immunology 182, no 1_Supplement (1 avril 2009) : 50.41. http://dx.doi.org/10.4049/jimmunol.182.supp.50.41.
Texte intégralBarbieri, Alessandro, Marzia Dolcino, Elisa Tinazzi, Antonella Rigo, Giuseppe Argentino, Giuseppe Patuzzo, Andrea Ottria, Ruggero Beri, Antonio Puccetti et Claudio Lunardi. « Characterization of CD30/CD30L+Cells in Peripheral Blood and Synovial Fluid of Patients with Rheumatoid Arthritis ». Journal of Immunology Research 2015 (2015) : 1–10. http://dx.doi.org/10.1155/2015/729654.
Texte intégralRomagnani, Paola, Francesco Annunziato, Roberto Manetti, Carmelo Mavilia, Laura Lasagni, Cinzia Manuelli, Gabriella B. Vannelli et al. « High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus ». Blood 91, no 9 (1 mai 1998) : 3323–32. http://dx.doi.org/10.1182/blood.v91.9.3323.
Texte intégralRomagnani, Paola, Francesco Annunziato, Roberto Manetti, Carmelo Mavilia, Laura Lasagni, Cinzia Manuelli, Gabriella B. Vannelli et al. « High CD30 Ligand Expression by Epithelial Cells and Hassal's Corpuscles in the Medulla of Human Thymus ». Blood 91, no 9 (1 mai 1998) : 3323–32. http://dx.doi.org/10.1182/blood.v91.9.3323.3323_3323_3332.
Texte intégralWiley, S. R., R. G. Goodwin et C. A. Smith. « Reverse signaling via CD30 ligand. » Journal of Immunology 157, no 8 (15 octobre 1996) : 3635–39. http://dx.doi.org/10.4049/jimmunol.157.8.3635.
Texte intégralThèses sur le sujet "CD30L T cell"
Mühle, Kerstin. « Interaction of CD8+CD40L+ T cells with B cells ». Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19127.
Texte intégralCTLs are important for the elimination of infected and degenerated cells by inducing apoptosis of the target cells. Recently our group identified a sub-population of CD8+ T cells expressing CD40L instead of common CTL markers. To that date, transient CD40L expression on T cells has been only described as a function of activated CD4+ T cells, which displays this key molecule for CD4+ T cell mediated help by binding to the CD40 receptor on other immune cells. Particularly, CD40L signaling provided by CD4+ T cells is indispensable for T cell dependent B cell activation and GC responses, which generate B cells secreting high affinity antibodies that protect the host from invading pathogens. Due to its associated helper functions, this thesis aimed to dissect whether CD40L positive CD8+ T cells are restricted to cytotoxic killing or if this sub-population possesses similar properties as CD4+ T cells when interacting with B cells. In vitro co-culture experiments showed that 50% of murine antigen specific CD8+ T cells up-regulated CD40L upon activation by antigen presenting B cells. When compared to CD40L deficient CD8+ T cells, the interaction of CD8+ CD40L+ T cells induced remarkable changes in B cells on the RNA and protein level and triggered a B cell phenotype resembling that of B cells primed by CD4+ T cells. By the infection of mice with the B cell trophic virus MHV-68, it was found that E8IcrexCD40Lflox transgenic mice lacking CD40L only on matured CD8+ T cells, exhibited a significant decrease of GC B cells in superficial cervical lymph nodes at the acute state of infection compared to WT mice. A closer look into the memory B cell repertoire revealed a preferred usage of the murine IGHJ3 gene family that modifies the CDR3 and thus the recognition groove of the B cell antibody in E8IcrexCD40Lflox mice. In summary, this work provides sufficient evidence that CD8+ CD40L+ T cells adopt helper-like functions by supporting B cell activation and subsequent GC formation.
Abduh, Maisa. « Follicular CD4 T Cells Tutor CD8 Early Memory Precursors : an Initiatory Journey to the Frontier of B Cell Territory ». Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS371.
Texte intégralAntigen-specific CD8 T cells are involved in the adaptive immune response and play a critical role in protecting the host from infection by intracellular pathogens. This long-lasting protection depends on the generation of memory CD8+ T cell responses, which are highly functional in terms of frequency and functionality, after secondary infection.Following antigen activation, a naive CD8 T cell undergoes strong clonal expansion, generating a heterogeneous population of activated cells that is dominated, at the peak of expansion, by short-lived CD8 effectors (SLECs). This expansion is followed by a phase of drastic contraction through massive apoptosis. A few cells survive this contraction phase and eventually become highly competent memory cells. Precisely when and how these memory precursors (MPECs) are generated is largely unknown, and so are the subsequent steps of their maturation into fully functional memory cells. Help signals from CD4+ T cells are clearly required throughout the MPEC maturation process.Our team has previously shown that FoxP3+ regulatory CD4+ T cells (Tregs) favor MPECs maturation by limiting exposure to IL-2 and by providing inhibitory signals, but this is probably only one facet of the complex and multifaceted help provided by CD4+ T cells to MPEC, and Tregs act on pre-existing MPECs.B-cell memory and CD8+ T cell memory share some common features, such as the expression of the transcription factor Bcl-6. Tfh are major producers of the cytokine IL-21. The mechanisms by which Tfh induces Bcl-6 in B-cells need to be clarified, they might include IL-21 and CD40-CD40L.In this PhD project, we have investigated the potential role of Tfh on the initiation of CD8 memory differentiation, in transgenic mice models, allowing transient and selective depletion of Tfh cells, infected by recombinant Listeria monocytogenes-OVA.We have shown that as early as 2 days after infection, very early memory precursors can be identified by their expression of the chemokine receptor CXCR5. These early precursors, which have an effector phenotype, expand and temporarily migrate to the junction of T-cell and B-cell zones, where they interact with follicular CD4 T cells (Tfh) then lose their CXCR5 expression.Remarkably, this interaction with Tfh, hitherto considered as exclusive B-cell helpers, is required for memory precursors to become competent memory cells responsive to IL-21 and capable of mounting efficient cytotoxic secondary effector responses.This study thus unveils critical early steps in the generation of CD8 memory, identifies CXCR5 as the earliest known marker of CD8 memory precursors, reveals a major helper role for Tfh, and points to possible coordination, through Tfh, between the pathways of CD8 and B-cell memory generation. These findings may have implications for vaccine and immunotherapy design
Loyal, Lucie. « The molecular regulation of CD40L in CD8+ T cells ». Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20158.
Texte intégralThe T cell compartment consists of two major subsets with diverse assignments. CD4+ T cells express CD40L upon activation, a central co-stimulatory receptor to induce B cell mediated humoral immunity, activate APCs and prime efficient effector CD8+ T cell development (“helper function”). In contrast, cytotoxic CD8+ T cells are predetermined to kill infected or malignant cells directly. However, a fraction of CD8+ T cells expressing CD40L upon activation was identified. So far, it is not understood in CD8+ T cells a) how CD40L expression is regulated, b) when and how the ability of CD40L expression is implemented and c) what are the implications for the immune system. In this thesis, we found that CD40L expression is regulated by DNA-methylation of regulatory regions of the CD40LG locus in CD4+ as well as CD8+ T cells. The de-methylation of central elements is implemented in the thymus and increases with T cell maturation reflected by enhanced stability of CD40L expression. Elevated CD5 and NUR77 expression of CD40L+ CD8+ SP thymocytes suggests that high affine detection of self-peptides during positive selection in the thymus implements CD40L expression ability and predetermines the fate of the CD40L imprinted CD8+ T cells. CD40L+ naïve CD8+ T cells differ in their TCR repertoire from their CD40L- counterparts and preferentially mature into memory cell subsets with cytokine and chemokine receptor profiles of Tc2, Tc17 and Tc22 cells. With their non-cytotoxic phenotype and gene expression signatures, the CD40L+ memory CD8+ T cell subsets Tc2, Tc17 and Tc22 widely resemble helper CD4+ T cells and can be distinguished from classical cytotoxic Tc1 and Tc17+1 cells by their IL-6R and absent SLAMF7 expression and their skin migratory phenotype. Altogether, we demonstrate that from the earliest developmental stages in thymus onwards naive CD8+ T cells are not homogenous and the abilites to provide “CD40L based help” or “cytotoxicity mediated killing” are independent of the CD4+ or CD8+ T cell status. Cells with helper-type CD8+ T cell cytokine and gene-expression signatures were found at barrier sites (skin, lung) by us and others where they contribute to multiple autoinflammatory diseases. Therefore, this work insinuates the need to revisite CD8+ T cell capablities and function in immune responses.
Hirano, Ayumi. « T dependent B cell help in cattle : immunoregulatory function of interleukin-4 and CD40-CD40L interactions / ». free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841150.
Texte intégralSchubert, Lisa Ann. « Characterization of the transcriptional regulation of the human CD40L gene in CD4 T cells / ». Thesis, Connect to this title online ; UW restricted, 1998. http://hdl.handle.net/1773/8325.
Texte intégralMühle, Kerstin [Verfasser], Hans-Dieter [Gutachter] Volk, Andreas [Gutachter] Thiel et Ulf [Gutachter] Wagner. « Interaction of CD8+CD40L+ T cells with B cells / Kerstin Mühle ; Gutachter : Hans-Dieter Volk, Andreas Thiel, Ulf Wagner ». Berlin : Humboldt-Universität zu Berlin, 2018. http://d-nb.info/1185495924/34.
Texte intégralLoyal, Lucie [Verfasser], Andreas [Gutachter] Thiel, Chiara [Gutachter] Romagnani et Hans-Dieter [Gutachter] Volk. « The molecular regulation of CD40L in CD8+ T cells / Lucie Loyal ; Gutachter : Andreas Thiel, Chiara Romagnani, Hans-Dieter Volk ». Berlin : Humboldt-Universität zu Berlin, 2019. http://d-nb.info/1190641046/34.
Texte intégralHarlin, Helena. « TRAF4 and CD30/TRAF2 in normal T cell function / ». 2001. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3019923.
Texte intégralChen, Jui-Chieh, et 陳瑞傑. « The inhibition of T cell proliferation by CD30 expression on the Hodgkin’s cancer cell ». Thesis, 2003. http://ndltd.ncl.edu.tw/handle/49838763617401022976.
Texte intégral國立臺灣大學
生物化學暨分子生物學研究所
91
英文摘要 Hodgkin''s disease is a type of malignant lymphoma, characterized by the presence of abnormal cells, named Reed-Sternberg cells, in patient’s lymph nodes. CD30 was originally described as a marker of Hodgkin/Reed-Sternberg cells. CD30 and its cognate ligand, CD153, belong to members of the TNFR and TNF superfamilies, respectively. CD30 is expressed on the surface of Hodgkin/Reed-Sternberg (H-RS) cell lines (KM-H2), while expression of CD153 can be induced on the surface of peripheral blood T cells by anti-CD3 or PHA activation. In this study, we addressed the effect of CD30 reverse signaling on T cells. By co-cultures of KM-H2 and PBMC activated by anti-CD3 or PHA, we observed T cell proliferation was inhibited. The inhibition was not dependent on cytokines or substances released from KM-H2, because KM-H2 cells were fixed with paraformaldehyde before the co-culture. We further study the effect of CD30 on T cell proliferation with CD30-expressing Chinese Hamster Ovary (CHO) cells to. In the presence of CD30-positive CHO cells, PHA-treated PBMC failed to achieve significant proliferation. Similar effects were observed if PHA-treated PBMC were cultured in the medium containing chimeric CD30-Fc fusion proteins. Taken together, we discover the inhibitory effect of CD30 reverse signaling on CD153-positive T cells. Furthermore, in order to characterize the protein expression profile in response to CD30 reverse signaling, proteomic technology was used. Several candidate spots were found to be likely regulated by CD30 engagement. One of these spots was identified as Mn-SOD by the use of MALDI-TOF MS. We conclude that H-RS cells are able to inhibit the proliferation of activated T cells through the CD30-CD153 interaction, which may lead to a microenvironment in favor of the growth and survival of the tumor cells.
Boyle, Julia Katrina. « The role of CD30 in the regulation of T cell function ». Thesis, 2003. http://hdl.handle.net/2429/14546.
Texte intégralLivres sur le sujet "CD30L T cell"
Lucas, Carrie Lynn. Mechanisms of deletional tolerance of peripheral CD8⁺ T cells induced by anti-CD40L and allogeneic bone marrow transplantation. 2010.
Trouver le texte intégralChapitres de livres sur le sujet "CD30L T cell"
Kadin, Marshall E., et Francine Foss. « Primary Cutaneous and Systemic CD30+ T-cell Lymphoproliferative Disorders ». Dans T-Cell Lymphomas, 71–86. Totowa, NJ : Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-170-7_5.
Texte intégralKaudewitz, Peter, Iannis Anagnostopoulos, Michael Hummel et Harald Stein. « HTLV-1 Proviral Sequences in Cutaneous CD30-Positive T Large Cell Lymphomas ». Dans Basic Mechanisms of Physiologic and Aberrant Lymphoproliferation in the Skin, 195–204. Boston, MA : Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1861-7_14.
Texte intégralWood, G. S., J. W. Gould et A. C. Gilliam. « Primary cutaneous CD30+ large-cell lymphoma with natural killer-cell phenotype and the t(2;5) translocation ». Dans Cutaneous Lymphomas, 40–41. Heidelberg : Steinkopff, 2001. http://dx.doi.org/10.1007/978-3-642-57624-9_20.
Texte intégralKazlouskaya, V., J. Ho et O. E. Akilov. « Case 42. Primary cutaneous CD30 T-cell posttransplant lymphoproliferative disorder with δ expression ». Dans Cutaneous Lymphomas, 98–99. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-59129-8_42.
Texte intégral« CD30+ cutaneous large T-cell lymphoma ». Dans Dermatology Therapy, 120. Berlin, Heidelberg : Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_525.
Texte intégral« Cd30þ T-cell Lymphoproliferative Disorders Of The Skin ». Dans Cutaneous Lymphomas, 193–210. CRC Press, 2005. http://dx.doi.org/10.1201/9780849346033-33.
Texte intégralKadin, Marshall E. « Primary Cutaneous CD30-Positive T-Cell Lymphoproliferative Disorders ». Dans Hematopathology, 604–16. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-7216-0040-6.00039-3.
Texte intégral« Cd30-Positive Lymphoproliferative Disorders Including Lymphomatoid Papulosis, Borderline Cd30-Positive Lymphoproliferative Disease, Anaplastic Large Cell Lymphoma, and T-Cell-Rich Cd30-Positive Large B Cell Lymphoma ». Dans The Cutaneous Lymphoid Proliferations, 274–311. Hoboken, NJ, USA : John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118776193.ch13.
Texte intégralActes de conférences sur le sujet "CD30L T cell"
Rana, Seema, et Rajiv Tangri. « Anaplastic large cell lymphoma ALK negative vs. peripheral T cell lymphoma (NOS) - diagnostic dilemma ». Dans 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685354.
Texte intégralHeiser, Ryan A., Bryan M. Grogan, Luke S. Manlove et Shyra J. Gardai. « Abstract 1789 : CD30+T regulatory cells, but not CD30+CD8 T cells, are impaired following brentuximab vedotin treatment in vitro and in vivo ». Dans Proceedings : AACR Annual Meeting 2018 ; April 14-18, 2018 ; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1789.
Texte intégralWu, Yang, Dan Chen, Rong Ma, Jun-ying Zhang, Yuan Zhang, Hai-xia Cao, Zhuo Wang et al. « Abstract 1444 : The new therapy strategy for treatment of peripheral T cell lymphomas : CD30-targeted CAR-modified T cell therapy ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1444.
Texte intégralWu, Yang, Dan Chen, Rong Ma, Jun-ying Zhang, Yuan Zhang, Hai-xia Cao, Zhuo Wang et al. « Abstract 1444 : The new therapy strategy for treatment of peripheral T cell lymphomas : CD30-targeted CAR-modified T cell therapy ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1444.
Texte intégralEscribà-Garcia, Laura, Carmen Alvarez-Fernández, Ana Carolina Caballero, Rydzek Julian, Einsele Hermann, Jorge Sierra, Michael Hudecek et Javier Briones. « Abstract A028 : Memory stem T-cells expressing an optimized CD30-specific chimeric antigen receptor (CAR) efficiently eradicate peripheral T-cell lymphoma in vivo ». Dans Abstracts : Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference : Translating Science into Survival ; September 30 - October 3, 2018 ; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a028.
Texte intégralCaires, Elisana Maria Santos, Régis Resende Paulinelli, Miliana Tostes Lucatto, Eneida Ribeiro Marinho et Henrique Moura de Paula. « BREAST IMPLANT–ASSOCIATED ANAPLASTIC LARGE CELL LYMPHOMA (BIA-ALCL) : A CASE REPORT WITH ATYPICAL SYMPTOMS ». Dans Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2096.
Texte intégralTrella, Emanuele, Evangelos Panoupolos, Swantje Heidtmann, Nermin Raafat, Giulio Cesare Spagnoli et Paul Zajac. « Abstract 2883 : Improved generation of central memory CD8+ T cells with CD40L expressing recombinant vaccinia virus ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2883.
Texte intégralMerz, Christian, Jaromir Sykora, Viola Marschall, David M. Richards, Meinolf Thiemann, Harald Fricke, Oliver Hill et Christian Gieffers. « Abstract 1760 : The hexavalent CD40 agonist HERA-CD40L augments multi-level crosstalk between T cells and antigen-presenting cells ». Dans Proceedings : AACR Annual Meeting 2018 ; April 14-18, 2018 ; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1760.
Texte intégralKua, Lindsay, Chee Hoe Ng, Jin Wei Tan, Richard Ong, Cheah Chen Seh, Fiona Wong, Don Sim, Ivan David Horak, Lionel Low et Kar Wai Tan. « 240 Humanized CD30 chimeric antigen receptor T cells with a novel 4–1BB derived spacer have improved activity and safety against CD30-positive lymphomas ». Dans SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0240.
Texte intégralCho, Hyun-Il, Chung-Hyo Kang, Sang-Eun Lee, In-Sil Song, Jung-Min Ha, Hyun-Jung Sohn et Tai-Gyu Kim. « 250 Chimeric antigen receptors containing CD30-derived costimulatory domain elicit augmented T cell effector functions and anti-tumor efficacy ». Dans SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0250.
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