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Books on the topic 'CD8'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 May 2024

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1

Kay, Lyndsey Sara. Anti-B-cell lymphoma activity mediated by CD3+CD4-CD8- T cells activated in vitro or in vivo. Ottawa: National Library of Canada, 2003.

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2

McDonagh, Mark Christian. An investigation of CD8 T lymphocyte development and function. Manchester: University of Manchester, 1994.

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3

Negative immunoregulatory role of CD8 T cells in peripheral tolerance. [New York]: [Columbia University], 1993.

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4

Ford, Megan. The role and mechanism of B6/1pr TCR[alpha beta]+CD4-CD8- T cells in immune response regulation. Ottawa: National Library of Canada, 2001.

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5

Carabin Is a Negative Regulator of Cd8+ T-cell-mediated Anti-tumor Immunity. [New York, N.Y.?]: [publisher not identified], 2022.

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6

Dumont, Caroline R. Identifying the autoantigen of a diabetogenic CD8 T cell clone isolated from Young NOD mice. [New Haven, Conn: s.n.], 1999.

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7

G, Janossy, Autran B, Miedema F, Commission of the European Communities., European Federation of AIDS Research., and Medical Research Council (Great Britain), eds. Immunodeficiency in HIV infection and AIDS. Basel: Karger, 1992.

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8

Sondermann, Bernd. Parteienfamilie ohne Zusammenhalt?: Programmatische Gegenreden von CDU, CDA und Tories auf die neue Sozialdemokratie. Frankfurt am Main: Lang, 2006.

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9

Cdn. 2nd ed. Warszawa: Książka i Wiedza, 1987.

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10

David, Rees. CDT. Harlow: Longman, 1989.

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11

Coach Drivers Club of Great Britain. CDC yearbook. Yate: CDC, 1999.

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12

Schmid, Josef. Die CDU. Wiesbaden: VS Verlag für Sozialwissenschaften, 1990. http://dx.doi.org/10.1007/978-3-322-95555-5.

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13

Breitenbach, Carolin. Steuer-CDs. Göttingen: V&R unipress, 2017. http://dx.doi.org/10.14220/9783737006385.

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14

Association, Colour Dimensions. CDA directory. London (44 Rockley Rd, London, W14 0BT): Colour Dimensions Association, 1995.

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15

CDC WONDER. Atlanta, Ga: CDC, 1997.

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16

Good, Keith. Starting CDT. London: Heinemann Educational Books, 1987.

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17

Louis, Barfe, and Key Note Ltd, eds. CDs & tapes. Hampton: Key Note, 1997.

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18

de, Moura Hélène, ed. Les CDI. Paris: De Vecchi, 2001.

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19

Lieping, Chen, ed. The B7-CD28 family molecules. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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20

Nguyen, Thuy-Linh Thi. CD8+ cytotoxic T lymphocyte tolerance and immunity. 2002.

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21

Young, Kevin J. The role and mechanisms of CD3+CD4-CD8-regulatory T cells in the suppression of allogeneic immune responses. 2003.

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22

Datta, Syamal Kumar, Antonio La Cava, David A. Horwitz, and Ciriaco A. Piccirillo, eds. Generating and Sustaining Stable Autoantigen-specific CD4 and CD8 Regulatory T Cells in Lupus. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-788-7.

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23

Koh, Dow-Rhoon. The role of CD4+, CD8+ and CD4-8-T cells in murine experimental allergic encephalomyelitis and lupus. 1993.

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24

Schildknecht, Anita. Induction and tolerization of CD8⁺ T cell responses in vivo. 2007.

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25

Ghaffar-Sedeh, Maryam. The role of CD8+ T cell recognition pathways in platelet alloimmunity. 2004.

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26

Gaiha, Gaurav D. Identification of CD8+ T cell host factors involved in HIV control. 2012.

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27

Cheung, Evelyn Joyce. Characterization of the CD8 T cell response to murine gammaherpesvirus 68 infection. 2012.

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28

Arosa, Fernando A., ed. On the Origin and Function of Human NK-like CD8+ T Cells: Charting New Territories. Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-396-2.

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29

Dimier-Poisson, Isabelle. Major Role for CD8+T Cells in the Protection Against Toxoplasma gondii Following Dendritic Cell Vaccination. INTECH Open Access Publisher, 2012.

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30

Vogl, Tim. Charakterisierung und Interaktion von CD8+ T-Lymphozyten und neutrophilen Granulozyten bei Patienten mit ANCA-assoziierter Vaskulitis. 2011.

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31

Veskler, Barbara A. New Research On Immunology. Nova Biomedical Books, 2005.

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32

Sterling, Katherine. The role of CD8+ T cells in the regulation of recipient immune responses induced by allogeneic platelet transfusions. 2004.

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33

Lucas, Carrie Lynn. Mechanisms of deletional tolerance of peripheral CD8⁺ T cells induced by anti-CD40L and allogeneic bone marrow transplantation. 2010.

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34

Bauer, Jan, and Christian G. Bien. Rasmussen Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0096.

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Rasmussen encephalitis (RE) is a rare epileptic disorder that is characterized by the presence of unihemispheric seizures coinciding with inflammation. The disease mostly presents in children. Clinically, patients often reach a residual stage with drug resistant seizures and severe neurological deficits. Pathologically, at this stage, the brain shows variable neuronal loss. The etiology is unknown but the infiltration of large numbers of CD8 positive T lymphocytes suggests that this is an autoimmune disease. Treatment consists of anti-inflammatory therapy (IVIG or tacrolimus), which, however, does not reduce the drug-resistant seizures. Therefore, hemisperectomy is the most effective treatment of RE.

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35

Panas, Michael William. Identification and elimination of immunosuppressive Mycobacterium bovis BCG genes to create novel rBCG vectors that generate increased CD8+ T cell responses. 2011.

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36

Hasbun, Rodrigo, Richard Dunham, Joseph S. Kass, Rituparna Das, Karen Nunez-Wallace, Lydia J. Sharp, and Doris Kung. HIV-Associated Neurocognitive Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0038.

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HIV causes a chronic form of encephalitis (HIVE) that is clinically characterized by either dementia or mild neurocognitive impairment. Since the introduction of antiretroviral therapy in 1996, the incidence of HIV dementia has decreased by 50%, but the prevalence of mild neurocognitive disorder has increased up to 39%. HIVE is the result of direct microglial infection, interruption of trophic factors, or caused by inflammatory cytokines. HIV enters the brain primarily by the “Trojan horse mechanism”; it is carried by monocytes and lymphocytes that cross the blood–brain barrier. HIV has a predilection for the basal ganglia, deep white matter, and hippocampus, resulting in a subcortical dementia. HIV dementia is a diagnosis of exclusion and other co-infections, cerebrovascular disease, malnutrition, and drug abuse should be ruled out before making the diagnosis. In patients receiving antiretroviral therapy with immunological response, a novel condition termed CD8+ T cell encephalitis was recently described.

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37

Colbert, Robert A., and Paul Bowness. Immune mechanisms: HLA-B27. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0006.

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HLA-B27 is present in the majority of patients with ankylosing spondylitis (AS). Although we have learned a considerable amount about the natural immunologic function of HLA class I proteins, this has not provided a definitive mechanism of AS pathogenesis. While HLA-B27 is adept at presenting antigenic peptides to CD8+ T cells, ‘arthritogenic’ peptides targeted by a cross-reactive T or natural killer cell response have not been described, nor have autoreactive T cells been found. Newer concepts have evolved based on the propensity of HLA-B27 to ‘misbehave’, both inside cells and on the cell surface. Misfolded HLA-B27 molecules may stimulate an endoplasmic reticulum stress response, promoting production of IL-23 and then IL-17 and related cytokines. Aberrant cell-surface HLA-B27 molecules are ligands for natural killer and related immunoreceptors, and recognition can lead to IL-17 proinflammatory responses. There is growing evidence to suggest that these aberrant behaviours contribute to AS pathogenesis.

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38

Cox, Josephine H., Stuart Z. Shapiro, Liza Dawson, Cynthia Geppert, Andrew M. Siegel, and M. Patricia D’Souza. Vaccines for The Prevention and Treatment of HIV Infection. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0032.

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While the HIV/AIDS pandemic continues, the overall incidence of HIV infections has fallen through use of antiretroviral therapy (ART) and multiple prevention modalities. To achieve a durable end to the pandemic and avoid the requirement for daily antiretroviral medication over a lifetime, a safe and effective prophylactic vaccine remains essential. This chapter reviews current advances in prophylactic and therapeutic HIV-1 vaccine strategies and the challenges that lie ahead. Recent success in isolation of potent broadly neutralizing antibodies (bnAbs) from infected individuals, the discovery of mechanisms of bnAb induction, and progress in understanding mechanisms of CD8 T-cell killing of HIV-infected cells and the structure of the HIV envelope trimer have opened new strategies for HIV vaccine design. On the therapeutic front, the persistence of HIV reservoirs remains a formidable obstacle to achieving sustained virological remission in HIV-infected individuals after ART is discontinued. Development of a new generation of immune-based therapeutic agents might contribute to a curative intervention. The chapter closes with an overview of ethical challenges in vaccine development and clinical testing.

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39

Marfil, Juan Ramón Larrubia. Análisis de la Respuesta Celular Cd8 Específica Contra el Virus B, en Función Del Control Viral y Grado de Inflamación Hepática, en la Infección Persistente Por el Virus B. Universidad Complutense de Madrid, Servicio de Publicaciones, 2005.

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40

Kerman, Joseph. Listen 4e Brief P & 3 CDs & Cdr Listen Charts. Bedford books, 2001.

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41

Guarido, Maura Duarte Moreira. CDD e CDU: uso e aplicabilidade para cursos de graduação em biblioteconomia. Faculdade de Filosofia e Ciências, 2010. http://dx.doi.org/10.36311/2010.978-85-98176-34-5.

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42

Grom, Alexei A., and Athimalaipet V. Ramanan. Macrophage activation syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0168.

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Macrophage activation syndrome (MAS) is a life-threatening condition caused by excessive activation and proliferation of T lymphocytes and haemophagocytic macrophages. Although MAS has been reported in association with almost any rheumatic disease, it is by far most common in systemic juvenile idiopathic arthritis. Flares of the underlying disease or infection are most common triggers of MAS. The pathognomonic feature of MAS is typically found in bone marrow: numerous, well-differentiated macrophagic histiocytes phagocytosing normal haematopoietic elements. The expansion of these histiocytes leads to a massive systemic inflammatory reaction associated with three cardinal clinical features: severe cytopenias, liver dysfunction, and coagulopathy consistent with disseminated intravascular coagulation. Clinically, MAS is strikingly similar to the autosomal recessive disorders collectively known as familial haemophagocytic lymphohistiocytosis (FHLH). FHLH has been associated with various genetic defects affecting the cytolytic pathway. Cytolytic function is profoundly depressed in MAS patients as well, and this abnormality is caused by both genetic and acquired factors. Studies in animals suggest that uncontrolled expansion of activated CD8+ T lymphocytes secreting cytokines that activate macrophages is central to the pathophysiology of haemophagocytic syndromes. Consistent with this view, the combination of steroids and ciclosporin, an immunosuppressant that preferentially inhibits T lymphocytes, is an effective treatment for the majority of MAS patients. Patients in whom MAS remains active despite this treatment present a serious challenge and require more aggressive immunosuppression. However, in MAS triggered by infection, the optimal level of immunosuppression is difficult to determine. As a result, reported mortality rates reach 20%.

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43

Certified Dental Technician(CDT) (Cdt). National Learning Corp, 2004.

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44

Steig, William. Cdb! Aladdin, 2003.

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45

Steig, William. Cdb! Simon & Schuster Books For Young Readers, 2022.

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46

Steig, William. Cdb! Aladdin, 1987.

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47

Steig, William. Cdb! Simon & Schuster Children's Publishing, 2000.

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48

Reports, Vault, and Vault Com Inc. CDI. Vault.com, 1998.

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49

Steig, William. Cdb. Tandem Library, 2003.

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50

Steig, William. Cdb. Sagebrush Education Resources, 1999.

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