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Books on the topic 'T cells responses'

Author: Grafiati
Published: 14 March 2023

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1

Tomkins, Paul Thomas. Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells. [s.l.]: typescript, 1989.

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2

Dockery, Dee. T cell responses to OspA, a candidate Lyme Disease vaccine. [New Haven, Conn: s.n.], 1993.

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3

Nagorsen, Dirk, and F. M. Marincola, eds. Analyzing T Cell Responses. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3623-x.

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4

Brouwenstijn, Nathalie. Characterization of the T-cell mediated immune response to renal cell carcinoma. [Leiden: University of Leiden], 1998.

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5

Regulatory T cells: Methods and protocols. [New York]: Humana Press, 2011.

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6

Liu, Yang. The costimulatory pathway for T cell response. Austin: R.G. Landes, 1994.

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7

L, Edelson Richard, ed. Antigen and clone-specific immunoregulation. New York, N.Y: New York Academy of Sciences, 1991.

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8

Na, Songqing, and Chandrasekar Venkataraman Iyer. Effector CD4+ T cells in health and disease 2007. Kerala, India: Transworld Research Network, 2007.

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9

Alexander, Michael A. Immune-based cancer treatment: The T lymphocyte response. Boca Raton, FL: CRC Press, 2011.

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10

O'Leary, Paula Frances Gerardine. T cell influences in antibody responses to lipopolysaccharides and polysaccharides. Birmingham: University of Birmingham, 2000.

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11

Alexander, Michael A. Immune-based cancer treatment: The T lymphocyte response. Boca Raton, FL: CRC Press, 2011.

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12

Ramage, Judith Margaret. Immunological memory: T cell responses to bacterial heat shock protein 60. Birmingham: University of Birmingham, 1997.

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13

Davies, Marie Louise. Autoantigen specific T cell responses in relation to systemic lupus erythematosus. Birmingham: University of Birmingham, 2000.

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14

Deane, Katherine Helen O'Leary. The characterisation of the t cell response to chlamydia trachomatis. Birmingham: University of Birmingham, 1996.

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15

Mawhinney, Heather. A molecular approach to the analysis of the T-cell response. [s.l: The Author], 1996.

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16

Rook, G. A. W. 1946- and Lightman Stafford L, eds. Steroid hormones and the T-cell cytokine profile. London: Springer, 1997.

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17

TH17 cells in health and disease. New York: Springer, 2011.

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18

Wiegers, Gerrit-Jan. Glucocorticoid hormone action in the immune system revisited. Delft: EburonP&L, 1995.

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19

Lau, Peggy. The role of 4-1BB/4-1BB ligand costimulation in T cell responses. Ottawa: National Library of Canada, 2001.

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20

H, Kiyono, and McGhee Jerry R, eds. Mucosal immunology: Intraepithelial lymphocytes. New York: Raven Press, 1994.

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21

Z, Atassi M., and Abbott Laboratories, eds. Immunobiology of proteins and peptides IV: T-cell recognition and antigen presentation. New York: Plenum Press, 1987.

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22

Leo, Sarah Elizabeth De. Human T cell response to substrate rigidity for design of improved expansion platform. [New York, N.Y.?]: [publisher not identified], 2014.

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23

D, Batista Facundo, and SpringerLink (Online service), eds. Immunological Synapse. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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24

B, Schook Lawrence, Tew John G, and International RES Symposium (1987 : Richmond, Va.), eds. Antigen presenting cells: Diversity, differentiation, and regulation : proceedings of a symposium held in Richmond, Virginia, March 26-29, 1987. New York: Liss, 1988.

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25

1943-, Watson James D., and Marbrook John, eds. Recognition and regulation in cell-mediated immunity. New York, N.Y: M. Dekker, 1985.

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26

R, Bock Gregory, Goode Jamie, and Novartis Foundation, eds. Generation and effector functions of regulatory lymphocytes. Chichester: John Wiley, 2003.

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27

Rao, Samhita Anand. Deconstructing T cell transcriptional heterogeneity and clonal dynamics in response to immune checkpoint blockade. [New York, N.Y.?]: [publisher not identified], 2022.

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28

Meding, Sally Joanna. CD4(plus) T cell effector mechanisms in the protective immune response to Plasmodium chabaudi chabaudi. Uxbridge: Brunel University, 1991.

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29

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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30

Gordin, Kaplan J., Green Doug R, and Bleackley R. Chris, eds. Cellular basis of immune modulation: Proceedings of the 19th International Leukocyte Culture Conference held at Banff Springs Hotel, Banff, Alberta, May 8-12, 1988. New York: A.R. Liss, 1988.

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31

Dhala, Ruwaida. An analysis of the in vivo SEB response in a T cell receptor scid transgenic mouse. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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32

Guide to signal pathways in immune cells. New York: Springer Verlag, 2009.

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33

Wardle, E. N. Guide to signal pathways in immune cells. New York: Springer Verlag, 2009.

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34

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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35

Killer cell dynamics: Mathematical and computational approaches to immunology. New York, NY: Springer, 2007.

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36

Eljaafari, Assia, and Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.
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37

(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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38

Marincola, Francesco M., and Dirk Nagorsen. Analyzing T Cell Responses: How to Analyze Cellular Immune Responses Against Tumor Associated Antigens. Springer London, Limited, 2006.

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39

Marincola, Francesco M., and Dirk Nagorsen. Analyzing T Cell Responses: How to Analyze Cellular Immune Responses Against Tumor Associated Antigens. Springer, 2010.

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40

Tuetken, Rebecca S. Characterization of murine culture-induced cells which suppress cytolytic T lymphocyte responses. 1989.

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41

Bins, Adriaan D. Induction and Analysis of Antigen-specific T cell Responses in Melanoma Patients and Animal Models. Amsterdam University Press, 2007.

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42

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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43

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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44

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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45

Breban, Maxime, and Hill Gaston. Immune mechanisms: adaptive immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0008.

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The role of adaptive immunity (i.e. the involvement of B and T lymphocytes) in the pathogenesis of axial spondyloarthritis has been investigated in both human disease and relevant animal models. Studies of B cell responses have not generally implicated an autoantibody in the disease, but there are abnormalities of antibody responses, particularly increased titres of antibodies to various gut bacteria. T cells are critical to the disease in animal models other than those where overexpression of a cytokine is engineered, suggesting that they are the drivers of the inflammatory response. There is convergent evidence from animal models, genetics in humans, and direct observation of human peripheral blood and joints to implicate T cells producing IL-17 under the influence of IL-23. These in turn may be responding to bacteria either in the gut or on the skin.
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46

Hayashi, Ren S. Regulatory T Cells. Nova Science Publishers, Incorporated, 2011.

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47

van der Vlag, Johan, and Jo H. M. Berden. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.
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48

Bhole, Malini. Hypersensitivity diseases. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0300.

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Hypersensitivity reactions are aberrant immune responses that are provoked by innocuous extrinsic or self-antigens, are mediated by B-cells or T-cells, and may result in tissue or organ damage. Coombs and Gell classified hypersensitivity reactions into four types, based on the different immune responses: type I, or immediate hypersensitivity; type II, or antibody-mediated (humoral) cytotoxicity; type III, or immune-complex disease; and type IV, or delayed hypersensitivity. This chapter reviews the clinical features, diagnosis, and management of hypersensitivity reactions.
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49

Stuart, Philip E., Lam C. Tsoi, Caely A. Hambro, and James T. Elder. Genetics of psoriasis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0005.

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Psoriasis is an immune-mediated inflammatory disease (IMID) characterized by skin inflammation, epidermal hyperplasia, increased risk of arthritis, and cardiovascular morbidity. Substantial evidence indicates that psoriasis is driven by abnormal interactions between cells of the innate and adaptive host defence systems, including keratinocytes, dendritic cells, and T-cells, resulting in a dysregulated immune response and markedly increased epidermal proliferation. The precise aetiology of psoriasis remains unknown. Here, we review how innate and adaptive host defence responses are regulated by genetic factors that modulate the overall risk of psoriasis and dictate whether the disease affects the skin and/or the joints. Specifically, we review the epidemiologic basis for considering psoriasis as a genodermatosis, summarize knowledge derived from linkage and association studies of cutaneous psoriasis (PsC) and psoriatic arthritis (PsA), and attempt to relate genetic and immunologic discoveries in a pathogenetic framework that may eventually allow prediction of the development of PsA in psoriatic individuals.
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50

McKisic, Maureen Denise. Characterization of ova-reactive and alloreactive CD4+ T cell subsets. 1992.

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