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Artykuły w czasopismach na temat "Tolérance des lymphocytes T"
Bonnefoy, Nathalie, Daniel Olive i Bernard Vanhove. "Les futures générations d’anticorps modulateurs des points de contrôle de la réponse immunitaire". médecine/sciences 35, nr 12 (grudzień 2019): 966–74. http://dx.doi.org/10.1051/medsci/2019193.
Pełny tekst źródłaHequet, Olivier, Marc Vocanson, Aurélie Guironnet-paquet, Audrey Nosbaum i Jean-François Nicolas. "Les lymphocytes T CD8+ suppresseurs jouent un rôle majeur dans la tolérance immunitaire induite par la photochimiothérapie extracorporelle". Annales de Dermatologie et de Vénéréologie 143, nr 12 (grudzień 2016): S426. http://dx.doi.org/10.1016/j.annder.2016.09.066.
Pełny tekst źródłaOchoa, Juan B., i Valeriya Makarenkova. "T lymphocytes". Critical Care Medicine 33, Suppl (grudzień 2005): S510—S513. http://dx.doi.org/10.1097/01.ccm.0000186788.71460.53.
Pełny tekst źródłaFabbri, M. "T lymphocytes". International Journal of Biochemistry & Cell Biology 35, nr 7 (lipiec 2003): 1004–8. http://dx.doi.org/10.1016/s1357-2725(03)00037-2.
Pełny tekst źródłaLotteau, V. "La période de tolérance néonatale existe-t-elle ?" médecine/sciences 12, nr 8-9 (1996): 983. http://dx.doi.org/10.4267/10608/859.
Pełny tekst źródłaRobijn, R. J., T. Logtenberg, L. J. J. M. Wiegman, G. P. Van Berge Henegouwen, R. W. Houwen i J. C. Koningsberger. "Intestinal T Lymphocytes". Scandinavian Journal of Gastroenterology 30, sup212 (styczeń 1995): 23–33. http://dx.doi.org/10.3109/00365529509090298.
Pełny tekst źródłaDegos, L. "Les lymphocytes T". médecine/sciences 3, nr 4 (1987): 229. http://dx.doi.org/10.4267/10608/3665.
Pełny tekst źródła&NA;. "Cytotoxic T lymphocytes". Reactions Weekly &NA;, nr 1085 (styczeń 2006): 12–13. http://dx.doi.org/10.2165/00128415-200610850-00037.
Pełny tekst źródłaMARTIN, STEPHEN, ED CANTIN i BARRY T. ROUSE. "Cytotoxic T Lymphocytes." Annals of the New York Academy of Sciences 532, nr 1 Cytotoxic T C (sierpień 1988): 257–72. http://dx.doi.org/10.1111/j.1749-6632.1988.tb36344.x.
Pełny tekst źródłaLangelot, M., K. Botturi-Cavaillès, D. Lair, F. Wessel, P. Germaud, A. Pipet i A. Magnan. "Lymphocytes T régulateurs". Revue Française d'Allergologie 50, nr 3 (kwiecień 2010): 98–101. http://dx.doi.org/10.1016/j.reval.2010.02.015.
Pełny tekst źródłaRozprawy doktorskie na temat "Tolérance des lymphocytes T"
De, Wit Dominique. "Tolérance immunologique induite: propriétés des lymphocytes T et des lymphocytes B". Doctoral thesis, Universite Libre de Bruxelles, 1991. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213001.
Pełny tekst źródłaLe, Saout Cécile. "Rupture de la tolérance périphérique en conditions de lymphopénie : coopération entre les cellules T CD8+ et CD4+". Montpellier 2, 2009. http://www.theses.fr/2009MON20097.
Pełny tekst źródłaThe onset of autoimmunity in patients as well as experimental rodent models frequently correlates with a lymphopenic state. In this condition, the immune system has evolved compensatory homeostatic mechanisms that induce quiescent naive T cells to proliferate and differentiate into memory-like lymphocytes even in the apparent absence of antigenic stimulation. Since memory T cells have less stringent requirements for activation than naïve cells, we hypothesized that auto-reactive T cells that arrive to secondary lymphoid organs in a lymphopenic environment could differentiate and bypass the mechanisms of peripheral tolerance. Utilizing a transgenic mouse system in which a model antigen is expressed in the pancreas, we have shown that potentially auto-reactive memory-like CD8+ T cells, generated under lymphopenic conditions, are not sufficient to induce auto-immunity because they are tolerized in the draining lymph nodes of the pancreas. Induction of self-reactivity required antigen-specific CD4+ T cell help. These helper cells promoted the further differentiation of memory-like CD8+ T cells into effectors in response to antigen cross-presentation with subsequent migration to the tissue of antigen expression where autoimmunity ensued. We also found that this effect is mediated by IL-2, a cytokine mainly produced by CD4 helper T cells. Thus, the cooperation between self-reactive memory-like CD4+ and CD8+ T cells under lymphopenic conditions overcomes cross-tolerance resulting in autoimmunity. These studies raise new perspectives, notably on cancer immunotherapy and the development of promising strategies optimizing anti-tumor T cell responses
Lemoine, Sébastien. "Étude du rôle du lymphocyte B dans la tolérance périphérique". Brest, 2011. http://www.theses.fr/2011BRES2308.
Pełny tekst źródłaNature has provided the immune system with numerous checkpoints controlling the maintenance of tolerance and the prevention of autoimmunity. The regulatory mechanisms operating in the periphery of the immune system are mediated mainly by a specific population of regulatory T cells considered as the main contributor to peripheral tolerance. In auto immunity, B cells are generally considered pathogenic since they release autoantibodies, that can cause damages to target tissues. However B cell depletion in several murine models of autoimmune diseases leads to a more severe pathology, giving B cells an unexpected regulatory role. Insights have been realized concerning the mechanism of action and the phenotype of this particular subset of regulatory B cells in mice and two subsets of IL-10 secreting B cells have been endowed with regulatory properties. However, despite increasing interest in regulatory B cell biology, the existence of an equivalent population in human is still a matter of controversy. The current study indicates that activated T cells can induce their own regulation by promoting the development of a B-cell dependent regulatory process. Regulatory B cells, identified by their expression of CD19high IgD+ CD24high CD38high CD5high, inhibit the proliferation and cytokine secretion of proinflammatory TH1 cells with the contribution of regulatory T cells, placing B cells at the center of immunosuppressive reactions. The assessment of this new regulatory function in autoimmune diseases shows that B-cell mediated immune regulation is deficient in Systemic Lupus Erythematosus
Poitrasson-Rivière, Maud. "Cellules T DC4+ FOXP3+ régulatrices et tolérance des lymphocytes T CD8+ à la périphérie". Paris 5, 2009. http://www.theses.fr/2009PA05T008.
Pełny tekst źródłaThe first part of this work showed, in an original mice model, that regulatory CD4+ T cells play an important role in preventing peripheral CD8+ T cell-mediated autoimmunity. We suggest that regulatory CD4+ Foxp3+ T cells induce the generation at the periphery of regulatory CD8+ T cells that can then regulate conventional CD8+ T cells activity. The second part of this work suggests strongly that self-recognition events are required to control autoreactive, potentially pathogenic, conventional T cells. Autoreactivity would thus be necessary for its own control
Billiard, Fabienne. "Etude de l'intéraction entre lymphocytes T régulateurs CD4+CD25+ et lymphocytes T effecteurs in vivo, chez la souris". Paris 6, 2007. http://www.theses.fr/2007PA066091.
Pełny tekst źródłaMarquez-Campos, Maria Elena. "Etude des mécanismes d'adaptation des lymphocytes T CD8+ dans la tolérance périphérique". Paris 6, 2004. http://www.theses.fr/2004PA066220.
Pełny tekst źródłaSantolaria, Thibault. "Induction de tolérance aux allogreffes d'organes solides par les lymphocytes T régulateurs CD4+ CD25+ FOXP3+". Toulouse 3, 2009. http://thesesups.ups-tlse.fr/498/.
Pełny tekst źródłaA major challenge in transplantation medicine is controlling the very strong immune responses to foreign antigens that are responsible for graft rejection. Although immunosuppressive drugs efficiently inhibit acute graft rejection, a substantial proportion of patients suffer chronic rejection that ultimately leads to functional loss of the graft. Induction of immunological tolerance to transplants would avoid rejection and the need for lifelong treatment with immunosuppressive drugs. Tolerance to self-antigens is ensured naturally by several mechanisms ; one major mechanism depends on the activity of regulatory T lymphocytes. We showed that in mice treated with clinically acceptable levels of irradiation, regulatory CD4+CD25+Foxp3+ T cells stimulated in vitro with alloantigens induced long-term tolerance to bone marrow and subsequent skin and cardiac allografts. Regulatory T cells specific for directly presented donor antigens prevented only acute rejection, despite hematopoietic chimerism. By contrast, regulatory T cells specific for both directly and indirectly presented alloantigens prevented both acute and chronic rejection. Our findings demonstrate the potential of appropriately stimulated regulatory T cells for future cell-based therapeutic approaches to induce lifelong mmunological tolerance to allogeneic transplants
Amiset, Laurent. "Identification de nouveaux inhibiteurs de l'activité suppressive des lymphocytes T régulateurs". Strasbourg, 2011. http://www.theses.fr/2011STRA6176.
Pełny tekst źródłaThe goal of my thesis project was to identify new inhibitors of CD4+ CD25+ FoxP3+ regulatory T lymphocytes (Treg) suppressive activity, which might facilitate immune responses against tumors and improve the efficacy of cancer-directed immunotherapeutic strategies. After having set up an in vitro model suitable for screening chemical and biological compound libraries, we identified out of 1754 molecules 56 candidate compounds inhibiting Treg-mediated suppression of CD4+ T cell proliferation. Treg were characterized during tumor progression in a mouse model of cancer immunotherapy. We showed that injections of the TLR1/2 ligand Pam3Cys associated with vaccination by an MVA vector encoding the tumor-associated antigen MUC1 prolong mouse survival and controls tumor progression. The combination of Pam3Cys with MVA-MUC1 enhances the MUC1-specific cellular response and protects effector T cells from Treg-mediated suppression, while inducing a Th17-type response which might be directly associated with the therapeutic benefit. Finally, the effect of a candidate compound selected from the library screening could be confirmed in vitro. Results from a first experiment in the RMA-MUC1 cancer model suggest that this compound potentiates the effect of the MVA-MUC1 vaccine and could therefore be useful for the immunotherapy of cancer
Villard, Marine. "Rôle de la profération induite par la lymphopénie dans la rupture de la tolérance périphérique des lymphocytes T CD8+". Thesis, Montpellier 2, 2013. http://www.theses.fr/2013MON20172/document.
Pełny tekst źródłaThe immune system has evolved multiple mechanisms of peripheral tolerance to control CD8+ T cell responses and to prevent autoimmunity. However, they also represent a barrier for the development of cytotoxic responses against tumors. Lymphodepleting protocols are currently used as adjuvants for adoptive cytotoxic T cell immunotherapy because they enhance their potency. These protocols are thought to promote the breakdown of peripheral CD8+ T cell tolerance. Under acute lymphopenic conditions, naive T cells proliferate, in the apparent absence of antigenic stimulation at least in part due to a greater availability of the cytokine IL-7. Proliferating CD8+ T cells acquire a phenotype and functionality that is similar to memory cells and are termed memory-like cells. Since memory cells have a lower activation threshold than naïve cells, it has been proposed that differentiation of potentially autoreactive CD8+ T cells into memory-like cells under lymphopenic conditions could drive the breakdown of peripheral tolerance. Here we studied whether lymphopenia induced proliferation and differentiation are required for the breakdown of CD8+ T cell cross-tolerance in irradiated transgenic mice expressing a model antigen in the beta cells of the pancreas. Surprisingly, we found that blocking lymphopenia-induced proliferation and differentiation into memory-like cells did not prevent self-reactivity. CD8+ T cells that did not differentiate into memory-like cells still became effectors upon antigen cross-presentation and migrated to the site of antigen expression. Nonetheless, LIP did enhance CD8+ T cell mediated self-reactivity at low T cell frequencies. This effect could not be explained by a Treg imbalance but by a net increase in autoreactive CD8+ T cell numbers. Thus, although LIP enhances CD8+ T cell anti-self responses, differentiation into memory-like cells is not essential for the breakdown of cross-tolerance under the lymphopenic conditions provided by irradiation
Thebault, Paméla. "Identification et étude de nouveaux médiateurs de la tolérance à l'allogreffe". Nantes, 2009. https://archive.bu.univ-nantes.fr/pollux/show/show?id=97f09501-6100-4061-be2f-e8a6e04ef996.
Pełny tekst źródłaThe understanding of immunological mechanisms leading to allograft tolerance represents a major issue to improve the success of organ transplantation. During my Ph. D, we have investigated news mediators of allograft tolerance in rat. In a model of tolerance induced by treatment with an analog of deoxyspergualin (LF15-0195), the team used DNA microarrays to identify mechanisms linked to tolerance and has observed a high expression of IDO and IFNγ. We have shown that CD4+CD25+ regulatory T cells accumulated in allograft expressed IFNγ and induced the expression of IDO in graft endothelial cells. So, these two molecules are necessary to tolerance. Moreover, we have identified CLEC-1, a C-type lectin receptor, as overexpressed in graft endothelial and myeloid cells of tolerated allograft. Then, we have shown that CLEC-1 expression is decreased by inflammatory stimuli and increased by tolerogenic molecules. At last, we have shown that CLEC-1 decreases Th17 differentiation, modulating suppression mediated by regulatory T cells. The role of IFNγ has also been demonstrated in another model of tolerance induced by the injection of autologous immature dendritic cells in combination with a suboptimal treatment with LF15-0195. We have demonstrated that inhibition of IFNγ abrogates induction of tolerance. Moreover, we have shown that double negative T cells are responsible of IFNγ production in the spleen of tolerant recipients. Interestingly, this production is dependent of EBI3 secreting by immature dendritic cells. All of these results contributed to identify new mediators of tolerance which will be able to be used as therapeutic tools to induce allograft tolerance
Książki na temat "Tolérance des lymphocytes T"
Celada, Franco, i Benvenuto Pernis, red. T Lymphocytes. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1.
Pełny tekst źródłaDebré, P. Clonage des lymphocytes T. Paris: Societé française d'immunologie, 1989.
Znajdź pełny tekst źródłaFranco, Celada, Pernis Benvenuto i North Atlantic Treaty Organization. Scientific Affairs Division., red. T Lymphocytes: Structure, functions, choices. New York: Plenum Press, 1992.
Znajdź pełny tekst źródłavon, Boehmer Harald, i Haas Werner, red. T cell clones. Amsterdam: Elsevier, 1985.
Znajdź pełny tekst źródłaCarton, Janet. Heterogeneity of Human Intestinal T Lymphocytes. Dublin: University College Dublin, 1998.
Znajdź pełny tekst źródłaAllen, Margaret Elizabeth. Intracellular signalling in rheumatoid T lymphocytes. Birmingham: University of Birmingham, 1996.
Znajdź pełny tekst źródłaCharles, Snow E., red. Handbook of B and T lymphocytes. San Diego: Academic Press, 1994.
Znajdź pełny tekst źródłaMarc, Feldmann, Lamb Jonathan R i Owen M. J, red. T cells. New York: Wiley, 1989.
Znajdź pełny tekst źródłaH, Kiyono, i McGhee Jerry R, red. Mucosal immunology: Intraepithelial lymphocytes. New York: Raven Press, 1994.
Znajdź pełny tekst źródła1956-, Zhang Jingwu, i Cohen Irun R, red. T-cell vaccination. New York: Nova Biomedical Books, 2008.
Znajdź pełny tekst źródłaCzęści książek na temat "Tolérance des lymphocytes T"
Wardle, E. Nigel. "T Lymphocytes". W Guide to Signal Pathways in Immune Cells, 247–92. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-538-5_13.
Pełny tekst źródłaRotte, Anand, i Madhuri Bhandaru. "T-Lymphocytes". W Immunotherapy of Melanoma, 167–98. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48066-4_7.
Pełny tekst źródłaBoitel, Brigitte, Myriam Ermonval, Ulrich Blank i Oreste Acuto. "T-Cell Antigen and MHC Recognition: Molecular Analysis of Human α/β TCR Specific for a Tetanus Toxin-Derived Peptide". W T Lymphocytes, 1–16. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_1.
Pełny tekst źródłaHannestad, Kristian. "On the Antigenicity of Antibody Idiotypes". W T Lymphocytes, 97–104. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_10.
Pełny tekst źródłaPernis, Benvenuto. "Idiotype Interactions between T Cells". W T Lymphocytes, 105–10. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_11.
Pełny tekst źródłaZanetti, Maurizio. "A Network of Self Interactions". W T Lymphocytes, 111–20. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_12.
Pełny tekst źródłaZaghouani, Habib, i Constantin Bona. "Stimulation of Lymphocytes by Anti-Idiotypes Bearing the Internal Image of Viral Antigens". W T Lymphocytes, 121–33. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_13.
Pełny tekst źródłaTada, Tomio, Tadahiro Inoue, Shuichi Kubo i Yoshihiro Asano. "Cloned Suppressor T Cells --- Their Identity, Functions, and Mediators". W T Lymphocytes, 135–44. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_14.
Pełny tekst źródłaHeber-Katz, Ellen. "The Autoreactive T Cell Receptor: Structure and Biological Activity". W T Lymphocytes, 145–51. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_15.
Pełny tekst źródłaJoseph, Sarah, Geoffrey Butcher, William Smith i Joyce Baird. "The Relationship between Diabetes and Lymphopenia in the BB Rat". W T Lymphocytes, 153–61. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_16.
Pełny tekst źródłaStreszczenia konferencji na temat "Tolérance des lymphocytes T"
Chen, Jianjun, Xianqing Luo, Jun Wang, Honghua Liao, Wenli Zhou, Ling Zhang, Heyou Han i Jun Yu. "Theoretical Analysis of T-lymphocytes Electroporation Model". W 2008 International Conference on Biomedical Engineering And Informatics (BMEI). IEEE, 2008. http://dx.doi.org/10.1109/bmei.2008.149.
Pełny tekst źródłaPatel, Shashank, Madhusudhanan Sukumar, Douglas Palmer, Rahul Roychoudhari, Rabindra Roy, Andre Nussenzweig i Nicholas Restifo. "Abstract 1347: Genomic stress in antigen experienced T-lymphocytes". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1347.
Pełny tekst źródłaRyan, RM, Q. Ahmed, CA D'Angelis, VH Kumar, S. Lakshminrusimha, LA Metlay, H. Wang i GS Pryhuber. "CD8+ T-Lymphocytes in Infants with Bronchopulmonary Dysplasia (BPD)." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5976.
Pełny tekst źródłaGiubileo, Gianfranco, Agostina Congiu Castellano, Silvia Gaudenzi, Paola Grimaldi, Deleana Pozzi i Adriana Puiu. "UV-B radiation induced effects on human T-lymphocytes". W SPIE Proceedings, redaktor Valentin I. Vlad. SPIE, 2007. http://dx.doi.org/10.1117/12.757866.
Pełny tekst źródłaJoseph, Robiya, Rama Soundararajan, Suhas Vasaikar, Fei Yang, Sevinj Isgandarova, Lin Tian, Monika Haemmerle i in. "Abstract 3761: Regulation of metastasis by CD8 T lymphocytes". W 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.am2019-3761.
Pełny tekst źródłaMioara, B., i A. Isac. "THU0098 Modification of t-lymphocytes subsets in rheumathoid arthritis". W Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.975.
Pełny tekst źródłaJoseph, Robiya, Rama Soundararajan, Suhas Vasaikar, Fei Yang, Sevinj Isgandarova, Lin Tian, Monika Haemmerle i in. "Abstract 3761: Regulation of metastasis by CD8 T lymphocytes". W 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.sabcs18-3761.
Pełny tekst źródłaMinagawa, Atsutaka, Akitsu Hotta, Yohei Kawai, Yutaka Yasui, Yasushi Uemura, Masaki Yasukawa, Tetsuya Nakatsura i Shin Kaneko. "Abstract 3585: T cell receptor-stabilized regenerated CD8ab cytotoxic T lymphocytes for cancer immunotherapy". W 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.am2018-3585.
Pełny tekst źródłaLungarella, Giuseppe, Giovanna De Cunto, Benedetta Lunghi, Barbara Bartalesi, Eleonora Cavarra, Silvia Fineschi, Cristina Ulivieri i Monica Lucattelli. "T lymphocytes in cigarette-smoke induced-emphysema and bronchial remodelling". W ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa4662.
Pełny tekst źródłaLo Re, Sandra, Marylène Lecocq, Francine Uwambayinema, Yousof Yakoub, Monique Delos, Jean-Baptiste Demoulin, Sophie Lucas i in. "PDGF-Producing CD4+ Foxp3+ Regulatory T Lymphocytes Promote Lung Fibrosis". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5552.
Pełny tekst źródłaRaporty organizacyjne na temat "Tolérance des lymphocytes T"
Minev, Boris R. Induction of Cytotoxic T Lymphocytes for Immunotherapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2003. http://dx.doi.org/10.21236/ada418851.
Pełny tekst źródłaAlbertini, R. J. The development of in vitro mutagenicity testing systems using t-lymphocytes. Office of Scientific and Technical Information (OSTI), luty 1998. http://dx.doi.org/10.2172/615639.
Pełny tekst źródłaAlbertini, R. J. The development of in vitro mutagenicity testing systems using T-lymphocytes. Office of Scientific and Technical Information (OSTI), maj 1992. http://dx.doi.org/10.2172/7049865.
Pełny tekst źródłaMekova, Ralitsa V., Spaska S. Lesichkova, Adelina D. Tsakova, Julieta Z. Bakalova, Deniz Bakalov i Mihail Boyanov. Circulating CD3(+)CD4(+)CD28(‒) T Lymphocytes in Patients with Autoimmune Thyroiditis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, maj 2020. http://dx.doi.org/10.7546/crabs.2020.05.14.
Pełny tekst źródłaAlbertini, R. J. The development of in vitro mutagenicity testing systems using T-lymphocytes. Office of Scientific and Technical Information (OSTI), maj 1993. http://dx.doi.org/10.2172/6238540.
Pełny tekst źródłaAlbertini, R. The development of in vitro mutagenicity testing systems using T-lymphocytes. Office of Scientific and Technical Information (OSTI), czerwiec 1990. http://dx.doi.org/10.2172/6748925.
Pełny tekst źródłaMalek, Thomas. Enhancing the Anti-Tumor Activity of breast Cancer-Specific Cytotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2000. http://dx.doi.org/10.21236/ada392196.
Pełny tekst źródłaHogan, Kevin T. Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cylotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, listopad 2008. http://dx.doi.org/10.21236/ada510798.
Pełny tekst źródłaHogan, Kevin T. Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cytotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, listopad 2006. http://dx.doi.org/10.21236/ada462674.
Pełny tekst źródłaHogan, Kevin T. Identification and Characterization of Ovarian Carcinoma Peptide Epitopes Recognized by Cytotoxic T Lymphocytes. Fort Belvoir, VA: Defense Technical Information Center, listopad 2007. http://dx.doi.org/10.21236/ada482936.
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